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Journal articles on the topic 'Uterine myometrium'
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1
Paul, Emmanuel N., Gregory W. Burns, Tyler J. Carpenter, Joshua A. Grey, Asgerally T. Fazleabas, and Jose M. Teixeira. "Transcriptome Analyses of Myometrium from Fibroid Patients Reveals Phenotypic Differences Compared to Non-Diseased Myometrium." International Journal of Molecular Sciences 22, no. 7 (March 31, 2021): 3618. http://dx.doi.org/10.3390/ijms22073618.
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Uterine fibroid tissues are often compared to their matched myometrium in an effort to understand their pathophysiology, but it is not clear whether the myometria of uterine fibroid patients represent truly non-disease control tissues. We analyzed the transcriptomes of myometrial samples from non-fibroid patients (M) and compared them with fibroid (F) and matched myometrial (MF) samples to determine whether there is a phenotypic difference between fibroid and non-fibroid myometria. Multidimensional scaling plots revealed that M samples clustered separately from both MF and F samples. A total of 1169 differentially expressed genes (DEGs) (false discovery rate < 0.05) were observed in the MF comparison with M. Overrepresented Gene Ontology terms showed a high concordance of upregulated gene sets in MF compared to M, particularly extracellular matrix and structure organization. Gene set enrichment analyses showed that the leading-edge genes from the TGFβ signaling and inflammatory response gene sets were significantly enriched in MF. Overall comparison of the three tissues by three-dimensional principal component analyses showed that M, MF, and F samples clustered separately from each other and that a total of 732 DEGs from F vs. M were not found in the F vs. MF, which are likely understudied in the pathogenesis of uterine fibroids and could be key genes for future investigation. These results suggest that the transcriptome of fibroid-associated myometrium is different from that of non-diseased myometrium and that fibroid studies should consider using both matched myometrium and non-diseased myometrium as controls.
2
Abramchenko, V. V. "The phenomenon of reversible myometrial dysfunction and delayed rehabilitation of uterine contractive ability." Journal of obstetrics and women's diseases 50, no. 2 (December 30, 2021): 55–57. http://dx.doi.org/10.17816/jowd89489.
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The author introduces the conception o f potentially reversible myometrial dysfunction with unaffected main physiological function o f myometrium (viability o f myometrium). This dysfunction is connected with the disturbances o f uterine haemodynamics. The phenomenon o f reversible myometrial dysfunction reflects the process o f prolonged decreased contractile ability o f the uterus.The therapy o f reversible myometrial dysfunction phenomenon should be directed to blood flow restoration under the conditions o f uterine hypoperfusion.The special treatment is not required fo r myometrium with reserved main physiological functions (tonus, excitability) because restoration o f myometrial contractile ability improves spontaneously in case o f blood flow restoration.With the aim o f prophylaxis o f myometrial dysfunction and delayed rehabilitation o f the uterine contractile function administration o f Ca antagonists, beta-adrenomymetics, antioxidants and preparations, which improve myometrial metabolic processes, is recommended before the expected delivery.
3
Mehasseb, Mohamed K., S. C. Bell, and M. A. Habiba. "The effects of tamoxifen and estradiol on myometrial differentiation and organization during early uterine development in the CD1 mouse." REPRODUCTION 138, no. 2 (August 2009): 341–50. http://dx.doi.org/10.1530/rep-09-0054.
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We used a neonatal mouse model to examine the histogenesis of uterine adenomyosis, and to test whether adenomyosis is due to an abnormality in myometrial differentiation, or in extracellular matrix proteins expression. We also studied the effects of tamoxifen and estradiol on uterine development, myometrial differentiation, and organization. Female CD1 pups were treated with oral tamoxifen (1 mg/kg) (n=27) or estradiol (0.1 mg/kg) (n=24) from age 1 to 5 days. Uteri from control (n=27) and treated mice were obtained on days 2, 5, 10, 15, and 42 of age. We examined the sections histologically, using image analysis and immunohistochemistry for α-smooth muscle actin (α-SMA), desmin, vimentin, laminin, fibronectin, and estrogen receptor-α. Following tamoxifen exposure, all uteri showed adenomyosis by 6 weeks of age (seen as early as day 10). The inner myometrium showed thinning, lack of continuity, disorganization, and bundling. α-SMA expression was normal. Desmin expression normally showed a wave of maturation that was absent in tamoxifen-treated mice. In the estradiol group, adenomyosis was not observed. All uterine layers were normally developed, but hypertrophied. The inner myometrium retained its circular arrangement. There was no difference in the localization of laminin or fibronectin between groups (laminin expression was reduced in the tamoxifen treated uteri). Vimentin could not be detected in all groups. Our results suggest that the development of the inner myometrium is particularly sensitive to estrogen antagonism, and can be affected by steroid receptors modulation. Disruption of the inner myometrium may play a role in the development of uterine adenomyosis.
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White, B. G., and D. J. MacPhee. "Distension of the uterus induces HspB1 expression in rat uterine smooth muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 5 (November 2011): R1418—R1426. http://dx.doi.org/10.1152/ajpregu.00272.2011.
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The uterine musculature, or myometrium, demonstrates tremendous plasticity during pregnancy under the influences of the endocrine environment and mechanical stresses. Expression of the small stress protein heat shock protein B1 (HspB1) has been reported to increase dramatically during late pregnancy, a period marked by myometrial hypertrophy caused by fetal growth-induced uterine distension. Thus, using unilaterally pregnant rat models and ovariectomized nonpregnant rats with uteri containing laminaria tents to induce uterine distension, we examined the effect of uterine distension on myometrial HspB1 expression. In unilaterally pregnant rats, HspB1 mRNA and Ser15-phosphorylated HspB1 (pSer15 HspB1) protein expression were significantly elevated in distended gravid uterine horns at days 19 and 23 (labor) of gestation compared with nongravid horns. Similarly, pSer15 HspB1 protein in situ was only readily detectable in the distended horns compared with the nongravid horns at days 19 and 23; however, pSer15 HspB1 was primarily detectable in situ at day 19 in membrane-associated regions, while it had primarily a cytoplasmic localization in myometrial cells at day 23. HspB1 mRNA and pSer15 HspB1 protein expression were also markedly increased in ovariectomized nonpregnant rat myometrium distended for 24 h with laminaria tents compared with empty horns. Therefore, uterine distension plays a major role in the stimulation of myometrial HspB1 expression, and increased expression of this small stress protein could be a mechanoadaptive response to the increasing uterine distension that occurs during pregnancy.
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Zaitseva, Marina, Sarah J. Holdsworth-Carson, Luke Waldrip, Julia Nevzorova, Luciano Martelotto, Beverley J. Vollenhoven, and Peter A. W. Rogers. "Aberrant expression and regulation of NR2F2 and CTNNB1 in uterine fibroids." REPRODUCTION 146, no. 2 (August 2013): 91–102. http://dx.doi.org/10.1530/rep-13-0087.
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Uterine fibroids are the most common benign tumour afflicting women of reproductive age. Despite the large healthcare burden caused by fibroids, there is only limited understanding of the molecular mechanisms that drive fibroid pathophysiology. Although a large number of genes are differentially expressed in fibroids compared with myometrium, it is likely that most of these differences are a consequence of the fibroid presence and are not causal. The aim of this study was to investigate the expression and regulation of NR2F2 and CTNNB1 based on their potential causal role in uterine fibroid pathophysiology. We used real-time quantitative RT-PCR, western blotting and immunohistochemistry to describe the expression of NR2F2 and CTNNB1 in matched human uterine fibroid and myometrial tissues. Primary myometrial and fibroid smooth muscle cell cultures were treated with progesterone and/or retinoic acid (RA) and sonic hedgehog (SHH) conditioned media to investigate regulatory pathways for these proteins. We showed that NR2F2 and CTNNB1 are aberrantly expressed in fibroid tissue compared with matched myometrium, with strong blood vessel-specific localisation. Although the SHH pathway was shown to be active in myometrial and fibroid primary cultures, it did not regulateNR2F2orCTNNB1mRNA expression. However, progesterone and RA combined regulatedNR2F2mRNA, but notCTNNB1, in myometrial but not fibroid primary cultures. In conclusion, we demonstrate aberrant expression and regulation of NR2F2 and CTNNB1 in uterine fibroids compared with normal myometrium, consistent with the hypothesis that these factors may play a causal role uterine fibroid development.
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Kim, Byoung Ywong, Chi-Heum Cho, Dae-Kyu Song, Kyo-Cheol Mun, Seong-Il Suh, Sang-Pyo Kim, Dong-Hoon Shin, et al. "Ciglitizone inhibits cell proliferation in human uterine leiomyoma via activation of store-operated Ca2+ channels." American Journal of Physiology-Cell Physiology 288, no. 2 (February 2005): C389—C395. http://dx.doi.org/10.1152/ajpcell.00154.2004.
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This study investigated the acute effects of a peroxisome proliferator-activated receptor (PPAR)-γ ligand, ciglitizone, on cell proliferation and intracellular Ca2+ signaling in human normal myometrium and uterine leiomyoma. Changes in intracellular Ca2+ concentration ([Ca2+]i) were measured with fura-2 AM, and cellular viabilities were determined by viable cell count and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide reduction assay. Ciglitizone (100 μM) induced greater inhibition of cell proliferation in uterine leiomyoma than in myometrium. Ciglitizone also dose-dependently increased [Ca2+]i in both myometrium and uterine leiomyoma; these [Ca2+]i increases were inhibited by PPAR-γ antagonists and raloxifene. Ciglitizone-induced [Ca2+]i increase showed only an initial peak in normal myometrial cells, whereas in uterine leiomyoma there was a second sustained [Ca2+]i increase as well. The initial [Ca2+]i increase in both myometrium and uterine leiomyoma resulted from the release of Ca2+ by the sarcoplasmic reticulum via activation of ryanodine receptors. The second [Ca2+]i increase was observed only in uterine leiomyoma because of a Ca2+ influx via an activation of store-operated Ca2+ channels (SOCCs). Cell proliferation was inhibited and secondary [Ca2+]i increase in uterine leiomyoma was attenuated by cotreatment of ciglitizone with a SOCC blocker, lanthanum. The results suggest that ciglitizone inhibits cell proliferation and increases [Ca2+]i through the activation of SOCCs, especially in human uterine leiomyoma.
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Kuzminykh, Tatyana U., Vera Yu Borisova, Igor P. Nikolayenkov, Georgy R. Kozonov, and Gulrukhsor Kh Tolibova. "Role of biologically active molecules in uterine contractile activity." Journal of obstetrics and women's diseases 68, no. 1 (March 20, 2019): 21–27. http://dx.doi.org/10.17816/jowd68121-27.
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Hypothesis/aims of study. Myometrial relaxation and contraction require synchronous cellular interactions. At present, it has been established that the coordination of myometrial contractile activity is carried out by a conduction system constructed from gap junctions with intercellular channels. There are no clinical data on inhibiting (nitric oxide synthase) and activating (connexin-43) factors of uterine contractile activity in the myometrium during pregnancy and parturition in the published literature. This study was undertaken to measure the expression levels of nitric oxide synthase, adhesion molecules CD51, CD61, and connexin-43 in the myometrium during pregnancy and parturition; and to assess the role of inhibitory and activating factors in the development of uterine contractile activity.
Study design, materials and methods. An immunohistochemical study of myometrial biopsy specimens obtained from the lower uterus segment during cesarean section was performed in eight women with a full-term physiological pregnancy, in another eight individuals in the active phase of uncomplicated parturition, and in eight patients with uterine inertia. Integrins (CD51 and CD61 proteins) were used as markers of cell adhesion. Localization and the number of intercellular contacts were assessed by measuring the expression level of connexin-43, with the intensity of oxidative processes assessed by nitric oxide synthase activity.
Results. In the myometrium, in the active phase of physiological parturition, a three-fold increase in the expression of activating (CD51, CD61, and connexin-43) factors of uterine contractile activity and a five-fold decrease in that of inhibitory (nitric oxide synthase) ones occur compared to those in full-term physiological pregnancy.
Conclusion. In the pathogenesis of uterine inertia and resistance to labor induction, an important role is played by the decreased expression of adhesion molecules (CD51, CD61) and connexin-43 and the increased expression of nitric oxide synthase in the myometrium.
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Yasuda, Katsuhiko, Tsuyoshi Nakamoto, Masahiro Yasuhara, Hidetaka Okada, Tatsuya Nakajima, Hideharu Kanzaki, Masatoshi Hori, and Hiroshi Ozaki. "Role of protein kinase Cβ in rhythmic contractions of human pregnant myometrium." Reproduction 133, no. 4 (April 2007): 797–806. http://dx.doi.org/10.1530/rep-06-0041.
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To assess the role of protein kinase Cβ (PKCβ) in human myometrial contractions during pregnancy, we evaluated the effect of a PKCβ inhibitor (LY333531) on the pregnant and nonpregnant myometrial contractions and compared the level of PKCβ in the pregnant myometrium with that in the nonpregnant myometrium. The effects of LY333531 on the myometrial contractions were examined by measuring contractile activity (frequency and amplitude). PKCβ in human myometrium was assessed at mRNA level using real-time PCR method. The characteristics of contractile activity were different between the pregnant and the nonpregnant myometrium. The amplitude of rhythmic contractions in the preterm and term myometrium was increased 2- to 2.5-fold when compared with that in the nonpregnant myometrium, but the frequency of rhythmic contractions was decreased by about half. LY333531 (10−6M) reduced the increased amplitude in the preterm and term myometrium by about 50%, and the inhibitory effects of LY333531 in the pregnant myometrium were significantly greater than that in the nonpregnant myometrium (about 50 vs 25%). However, the frequency in the pregnant and nonpregnant myometrium was not influenced by LY333531. Real-time PCR revealed a significant, five- to sevenfold increase in the expression of PKCβ mRNA in the preterm and term myometrium when compared with the nonpregnant myometrium. These findings suggest that the increased amplitude of human myometrial contractions during pregnancy is related to the increased level of PKCβ. A PKCβ inhibitor may reduce preterm uterine contractions and prevent preterm delivery.
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Vodstrcil, Lenka A., Mary E. Wlodek, and Laura J. Parry. "Effects of uteroplacental restriction on the relaxin-family receptors, Lgr7 and Lgr8, in the uterus of late pregnant rats." Reproduction, Fertility and Development 19, no. 4 (2007): 530. http://dx.doi.org/10.1071/rd07007.
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The peptide hormone relaxin stimulates uterine growth and endometrial angiogenesis and inhibits myometrial contractions in a variety of species. The receptor for relaxin is a leucine-rich repeat containing G-protein-coupled receptor Lgr7 (RXFP1) that is highly expressed in the myometrium of late pregnant mice, with a significant decrease in receptor density observed at term. The present study first compared the expression of Lgr7 with another relaxin-family receptor Lgr8 (RXFP2) in the uterus and placenta of late pregnant rats. The uterus was separated into endometrial and myometrial components, and the myometrium into fetal and non-fetal sites, for further analysis. We then assessed the response of these receptors to uteroplacental restriction (UPR). Expression of the Lgr7 gene was significantly higher in the uterus compared with the placenta. Within the uterus, on Day 20 of gestation, there was equivalent expression of Lgr7 in fetal and non-fetal sites of the myometrium, as well as in the endometrium v. myometrium. The second receptor investigated, Lgr8, was also expressed in the endometrium and myometrium, but at significantly lower levels than Lgr7. Bilateral ligation of the maternal uterine blood vessels on Day 18 of gestation resulted in uteroplacental restriction, a decrease in fetal weight and litter size, and a significant upregulation in uterine, but not placental, Lgr7 and Lgr8 gene expression in UPR animals compared with controls. These data suggest that both relaxin family receptors are upregulated in response to a reduction in uteroplacental blood flow in rats.
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Brenninkmeijer, CB, SA Price, A. Lopez Bernal, and S. Phaneuf. "Expression of G-protein-coupled receptor kinases in pregnant term and non-pregnant human myometrium." Journal of Endocrinology 162, no. 3 (September 1, 1999): 401–8. http://dx.doi.org/10.1677/joe.0.1620401.
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There is evidence for hormonal receptor desensitisation in human myometrium, but little is known about the mechanisms involved in the loss of myometrial response to agonists such as beta(2)-adrenergic agonists, prostaglandin gamma and oxytocin. It is well known that the receptors for these hormones are coupled to G-proteins. The first step of receptor desensitisation is the phosphorylation of activated receptors by a G-protein-coupled receptor kinase (GRK). GRKs are members of a multigene family and the various subtypes differ in their localisation, regulation and mode of action. We have used Western blotting and reverse transcription PCR to identify the GRKs present in human myometrium from pregnant and non-pregnant women as well as in cultured human myometrial cells. We have found that human myometrium expresses the GRK subtypes 2, 4gamma, 5 and 6. On the other hand, GRK3 and the isoforms GRK4alpha, beta and delta were not found in myometrial tissue. Our data indicate that GRK2 is only expressed in pregnant term myometrium and is not found in non-pregnant tissue. Moreover, GRK6 appears to be expressed at a much higher level in pregnant term tissue than in non-pregnant myometrium. Our observations suggest that GRK2 and GRK6 may contribute to the regulation of uterine contractility at term. Further work is necessary to determine whether GRKs and receptor desensitisation play a role in disorders of uterine contractility.
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Sawangjaroen, Kitja, and Kasorn Keereevong. "Spasmolytic Effect of Papaya (Carica papaya L.) Leave Alkaloid on Isolated Rat Myometrial Contraction in vitro." Trends in Sciences 19, no. 4 (February 15, 2022): 2684. http://dx.doi.org/10.48048/tis.2022.2684.
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This study aimed to investigate the action of crude alkaloid extract from papaya leaves (PA) on the isolated rat myometrium in vitro. The alkaloids were extracted from papaya leaves using conventional acid-base method. The myometrium strips were taken from female Wistar rats pretreated with diethylstilbestrol (100 mg) for 24 h before the experiment. A preliminary experiment has shown that PA had no effect on myometrial contraction. However, PA (10-6 - 10-3 gm/mL) significantly inhibited myometrium contraction pre-contracted with a depolarizing solution in a concentration-dependent fashion. PA (10-5, 3×10-5 or 10-4 gm/mL) or verapamil (10-9, 10-8 and 10-7 M) were able to inhibit the myometrial contractile response to CaCl2 (10-5 - 3×10-2 M) in Ca2+-free solution and cause a rightward shift of log concentration-response curve. PA also significantly inhibited myometrium contraction produced by oxytocin (1 mU/mL), ACh (3×10-5 M) and PGF2a (10-5 M). Furthermore, propranolol (10-7 M) caused no effect on uterine relaxation induced by PA (10-6 - 10-3 gm/mL), although it inhibited uterine relaxation induced by isoproterenol (10-10 - 10-5 M). These results indicated that PA was a uterine relaxant. Its mechanism of action may be unrelated to stimulation of b2-adrenergic receptors of the uterus. This action may be contributed to mainly the Ca2+ influx, possibly through voltage-operated Ca2+ channel on the plasma membrane, and to a lesser extent by a rise in Ca2+ release from internal storage. However, the action of PA at intracellular sites, downstream of Ca2+ influx such as the contractile machinery of the myometrium, cannot be excluded.
HIGHLIGHTS
Alkaloid extract from Carica papayaleaves has shown to be a uterine relaxant on isolated rat uterus in vitro
The alkaloid extract was able to inhibit uterine contraction stimulated by various uterine stimulants such as acetylcholine, oxytocinand prostaglandin F2alpha
The inhibition on uterine contraction may be due to the inhibition on calcium influx into the uterine muscle cells
GRAPHICAL ABSTRACT
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Yin, Zongzhi, Alaa A. Sada, Ossama M. Reslan, Neha Narula, and Raouf A. Khalil. "Increased MMPs expression and decreased contraction in the rat myometrium during pregnancy and in response to prolonged stretch and sex hormones." American Journal of Physiology-Endocrinology and Metabolism 303, no. 1 (July 1, 2012): E55—E70. http://dx.doi.org/10.1152/ajpendo.00553.2011.
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Normal pregnancy is associated with uterine relaxation to accommodate the stretch imposed by the growing fetus; however, the mechanisms underlying the relationship between pregnancy-associated uterine stretch and uterine relaxation are unclear. We hypothesized that increased uterine stretch during pregnancy is associated with upregulation of matrix metalloproteinases (MMPs), which in turn cause inhibition of myometrium contraction and promote uterine relaxation. Uteri from virgin, midpregnant ( day 12), and late-pregnant rats ( day 19) were isolated, and myometrium strips were prepared for measurement of isometric contraction and MMP expression and activity using RT-PCR, Western blot analysis, and gelatin zymography. Oxytocin caused concentration-dependent contraction of myometrium strips that was reduced in mid- and late-pregnant rats compared with virgin rats. Pretreatment with the MMP inhibitors SB-3CT (MMP-2/MMP-9 Inhibitor IV), BB-94 (batimastat), or Ro-28–2653 (cipemastat) enhanced contraction in myometrium of pregnant rats. RT-PCR, Western blot analysis, and gelatin zymography demonstrated increased mRNA expression, protein amount, and activity of MMP-2 and MMP-9 in myometrium of late-pregnant>midpregnant>virgin rats. Prolonged stretch of myometrium strips of virgin rats under 8 g basal tension for 18 h was associated with reduced contraction and enhanced expression and activity of MMP-2 and MMP-9, which were reversed by MMP inhibitors. Concomitant treatment of stretched myometrium of virgin rats with 17β-estradiol (E2), progesterone (P4), or E2+P4 was associated with further reduction in contraction and increased MMP expression and activity. MMP-2 and MMP-9 caused significant reduction of oxytocin-induced contraction of myometrium of virgin rat. Thus, normal pregnancy is associated with reduced myometrium contraction and increased MMPs expression and activity. The results are consistent with the possibility that myometrium stretch and concomitant increase in sex hormones during pregnancy are associated with increased expression/activity of specific MMPs, which in turn inhibit uterine contraction and promote uterine relaxation.
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Mignot, Thérèse-Marie, Brigitte Paris, Bruno Carbonne, Christian Vauge, Françoise Ferré, and Daniel Vaiman. "Corticotropin-releasing hormone effects on human pregnant vs. nonpregnant myometrium explants estimated from a mathematical model of uterine contraction." Journal of Applied Physiology 99, no. 3 (September 2005): 1157–63. http://dx.doi.org/10.1152/japplphysiol.00158.2005.
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In this paper, we applied a new theoretical model of uterine contraction to a large panel of human pregnant and nonpregnant myometrial strips, treated or not by corticotrophin-releasing hormone (CRH). This model is based on a fine analysis of the contraction curves. This analysis yielded four mathematical parameters (beta, theta, tau 1, and tau 2) related to excitability, duration of plateau phase, and time constants for relaxation describing, respectively, the different portions of the contraction cycle. This leads to specific differences in spontaneous contractile activity between pregnant and nonpregnant states. The relaxing effect of CRH in the pregnant state is presumably correlated with the origin of the strips (the lower uterine segment). Besides our observation of a specific receptor-dependent relaxing effect of CRH in both pregnant and nonpregnant myometrium, we could identify highly significant effects at given CRH concentration for beta in nonpregnant myometrium and for theta, tau 1, and tau 2 in pregnant myometrium. In addition, highly significant differences were found between pregnant and nonpregnant myometrium. Also, we discovered a strong correlation between theta and tau 1, specifically in the pregnant state. Although the biochemical signification of these results remains to be elucidated, they contribute to emphasize the complex network of CRH action at the myometrial level. Furthermore, our approach could pave the way toward a better analysis of the efficacy of the uterine contractile behavior.
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Jana, Barbara, Jarosław Całka, and Bartosz Miciński. "Regulatory Influence of Galanin and GALR1/GALR2 Receptors on Inflamed Uterus Contractility in Pigs." International Journal of Molecular Sciences 22, no. 12 (June 15, 2021): 6415. http://dx.doi.org/10.3390/ijms22126415.
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Uterine inflammation is a very common and serious pathology in domestic animals, the development and progression of which often result from disturbed myometrial contractility. We investigated the effect of inflammation on the protein expression of galanin (GAL) receptor subtypes (GALR)1 and GALR2 in myometrium and their role in the contractile amplitude and frequency of an inflamed gilt uterus. The gilts of the E. coli and SAL groups received E. coli suspension or saline in their uteri, respectively, and only laparotomy was performed (CON group). Eight days later, the E. coli group developed severe acute endometritis and lowered GALR1 protein expression in the myometrium. Compared to the pretreatment period, GAL (10−7 M) reduced the amplitude and frequency in myometrium and endometrium/myometrium of the CON and SAL groups, the amplitude in both stripes and frequency in endometrium/myometrium of the E. coli group. In this group, myometrial frequency after using GAL increased, and it was higher than in other groups. GALR2 antagonist diminished the decrease in amplitude in myometrium and the frequency in endometrium/myometrium (SAL, E. coli groups) induced by GAL (10−7 M). GALR1/GALR2 antagonist and GAL (10−7 M) reversed the decrease in amplitude and diminished the decrease in frequency in both examined stripes (CON, SAL groups), and diminished the drop in amplitude and abolished the rise in the frequency in the myometrium (E. coli group). In summary, the inflammation reduced GALR1 protein expression in pig myometrium, and GALR1 and GALR2 participated in the contractile regulation of an inflamed uterus.
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AG, Kedrova Genrikhovna, Levakov Aleksandrovich SA, Nechaeva Evgen'evna OE, Tazitdinov Khallilovich RH, and Chelnokova Nikolaevna NN. "ULTRASOUND CRITERIA FOR DIAGNOSIS AND MONITORING OF DRUG THERAPY OF COMBINED PROLIFERATIVE DISEASES OF THE UTERUS." Journal of Clinical Practice 5, no. 3 (September 15, 2014): 25–34. http://dx.doi.org/10.17816/clinpract5325-34.
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The aim of the paper was to evaluate the diagnostic accuracy of transvaginal tenderness-guided ultrasonography in the identification of location of genital endometriosis, endometrial hyperplasia and uterine fibroids before and after treatment dienogest. It is a selective progestin for the treatment of endometriosis. Adenomyosis was diagnosed when a poorly defined area of abnormal echo-texture (decreased or increased echogenicity, heterogeneous echotexture, myometrial cysts) presented in myometrium. Typical ultrasonic changes of efficacy were: homogeneity of myometrium; clear and intense contours of uterine fibroid with increased echogenicity; reduction of the echogenic endometrial stripe with the average echogenicity and clear lines of myo- and endometrium with a reduction in local blood. These criteria can be used to select non-surgical management of patients. In cases where a poorly defined area of abnormal echotexture (decreased or increased echogenicity, heterogeneous echotexture, myometrial cysts) did not change the surgery or the embolization of artery uterine is required. The preferred imaging modality for the evaluation of uterine on therapeutic alternatives to hysterectomy and myomectomy is transvaginal ultrasonography.
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Cramer, Stewart F., and Debra S. Heller. "Placenta Increta Presenting as Exaggerated Placental Site Reaction." Pediatric and Developmental Pathology 20, no. 2 (January 25, 2017): 152–57. http://dx.doi.org/10.1177/1093526616681939.
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Exaggerated placental site (EPS) is usually an incidental finding seen in curettings after an abortion. Placenta increta is, by definition, a disease that damages and destroys myometrium; however, prior literature has not paid sufficient attention to the role of myometrium in its pathogenesis and diagnosis. We present an unusual case of placenta increta in a hysterectomy performed for uterine perforation after curettage for the termination of pregnancy at 18 weeks. The initial histologic section of the implantation site suggested EPS. Actin stains showed degenerated inflamed muscle at the EPS-like site, keratin stains showed interstitial trophoblast in the zone of myometrial damage, and the wall of the corpus was grossly thinned under the placenta. The myometrial damage may have softened the wall, predisposing to uterine perforation by the curettage procedure.
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Nicoletti, J. G., B. G. White, E. I. Miskiewicz, and D. J. MacPhee. "Induction of expression and phosphorylation of heat shock protein B5 (CRYAB) in rat myometrium during pregnancy and labour." Reproduction 152, no. 1 (July 2016): 69–79. http://dx.doi.org/10.1530/rep-16-0092.
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During pregnancy the myometrium undergoes a programme of differentiation induced by endocrine, cellular, and biophysical inputs. Small heat shock proteins (HSPs) are a family of ten (B1–B10) small-molecular-weight proteins that not only act as chaperones, but also assist in processes such as cytoskeleton rearrangements and immune system activation. Thus, it was hypothesized that HSPB5 (CRYAB) would be highly expressed in the rat myometrium during the contractile and labour phases of myometrial differentiation when such processes are prominent. Immunoblot analysis revealed that myometrial CRYAB protein expression significantly increased from day (D) 15 to D23 (labour;P<0.05). In correlation with these findings, serine 59-phosphorylated (pSer59) CRYAB protein expression significantly increased from D15 to D23, and was also elevated 1-day post-partum (P<0.05). pSer59-CRYAB was detected in the cytoplasm of myocytes within both uterine muscle layers mid- to late-pregnancy. In unilaterally pregnant rats, pSer59-CRYAB protein expression was significantly elevated in the gravid uterine horns at both D19 and D23 of gestation compared with non-gravid horns. Co-immunolocalization experiments using the hTERT-human myometrial cell line and confocal microscopy demonstrated that pSer59-CRYAB co-localized with the focal adhesion protein FERMT2 at the ends of actin filaments as well as with the exosomal marker CD63. Overall, pSer59-CRYAB is highly expressed in myometrium during late pregnancy and labour and its expression appears to be regulated by uterine distension. CRYAB may be involved in the regulation of actin filament dynamics at focal adhesions and could be secreted by exosomes as a prelude to involvement in immune activation in the myometrium.
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Burroughs, KD, SR Howe, Y. Okubo, R. Fuchs-Young, D. LeRoith, and CL Walker. "Dysregulation of IGF-I signaling in uterine leiomyoma." Journal of Endocrinology 172, no. 1 (January 1, 2002): 83–93. http://dx.doi.org/10.1677/joe.0.1720083.
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IGF-I expression has been observed in human uterine leiomyomas. To examine whether autocrine IGF-I signaling plays a role in the growth of these tumors, we used an animal model of uterine leiomyoma (the Eker rat) to investigate regulation of IGF-I and the IGF-I receptor (IGF-IR) expression in tumors and normal myometrium. During the normal estrous cycle, myometrial IGF-I expression peaked on the day of proestrus when the rate of proliferation in this tissue is greatest. In leiomyomas, the expression of IGF-I was increased 7.5-fold compared with the age-matched normal tissue. The level of IGF-IR mRNA in both tumor and non-tumor tissues was found to inversely correlate with that of IGF-I. Changes observed in IGF-I signaling components correlated with the activation state of the signal-transducing protein insulin receptor substrate-1 (IRS-1). During diestrus and proestrus when IGF-I levels were increasing, tyrosine phosphorylation of IRS-1 was increased up to 5.7-fold in the normal myometrium relative to estrus, when IGF-I levels were the lowest. Additionally, IRS-1 phosphorylation was 4-fold greater in leiomyomas relative to age-matched normal myometrium. Autocrine stimulation of the IGF-IR may, therefore, play a role in regulating the normal growth of the myometrium, and dysregulation of IGF-I signaling could contribute to the neoplastic growth of uterine leiomyomas.
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Sharmazanova, О. P., I. N. Safonova, and Y. S. Mityakova. "Applicability of sonoelastography in leiomyoma and adenomyosis." Український радіологічний та онкологічний журнал 29, no. 1 (March 29, 2021): 78–88. http://dx.doi.org/10.46879/ukroj.1.2021.78-88.
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Background. Uterine leiomyoma and endometriosis are common gynecological diseases of women in childbearing potential. This fact necessitates developing an optimal protocol for examination of patients in order to implement an individual approach to treatment. Diagnosis of mixed forms of pathological myometrium conditions causes some difficulties. Elastography technique makes it possible to assess the density of the myometrium, which may be essential for differentiating the diagnosis of leiomyoma and adenomyosis in mixed forms.
Рurpose – to ascertain the potential of transvaginal ultrasound along with compression sonoelastography to determine the deformation coefficient in differential diagnosis of various pathological myometrium conditions.
Materials and methods. The paper presents the analysis of elastographic findings of the uterus in 155 women obtained via compression sonoelastography performed by means of HITACHI AVIUS device. Patients were divided into 4 groups: control, women with uterine leiomyoma, uterine adenomyosis, with combined leiomyoma and adenomyosis. The transabdominal/ transvaginal ultrasound findings were confirmed by histopathological examination. The standard point scale was used to determine the deformation coefficient.
Results. Elastographic characteristics were assessed in accordance with sonoelastography findings, i. e. deformation coefficients common in leiomyoma and adenomyosis. The maximum values of the deformation coefficient were obtained in leiomyoma (in an amount of 2 to 6.0 units). In case of diffuse or focal adenomyosis, the deformation coefficient was in an amount of 0.5 to 1.5 units indicating high myometrial elasticity vs the unchanged myometrium. For its part, in Group I (control), the deformation coefficient ranged from 1 to 1.7 units. High myometrial elasticity in adenomyosis vs the unchanged myometrium as well low elasticity or high density of the myometrium in leiomyoma were observed.
Conclusions. The deformation coefficients in patients with leiomyoma and adenomyosis and unchanged myometrium were obtained via ultrasound with compression sonoelastography and they made it possible to determine the degree of elasticity of the myometrium and its changes in the relevant pathology. Elastography is capable of identifying clear distinctive features of leiomyoma and adenomyosis. The coincidence of the diagnosis of adenomyosis based on elastography and histology is significant, but not optimal. The unchanged myometrium has a certain elasticity, which can be equated to a numerical value, i. e. the deformation coefficient, and this param changes in case of leiomyoma or adenomyosis, which makes it possible to differentiate these pathological conditions of the myometrium.
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Maxey, Antonina P., and Megan L. McCain. "Tools, techniques, and future opportunities for characterizing the mechanobiology of uterine myometrium." Experimental Biology and Medicine 246, no. 9 (February 7, 2021): 1025–35. http://dx.doi.org/10.1177/1535370221989259.
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The myometrium is the smooth muscle layer of the uterus that generates the contractions that drive processes such as menstruation and childbirth. Aberrant contractions of the myometrium can result in preterm birth, insufficient progression of labor, or other difficulties that can lead to maternal or fetal complications or even death. To investigate the underlying mechanisms of these conditions, the most common model systems have conventionally been animal models and human tissue strips, which have limitations mostly related to relevance and scalability, respectively. Myometrial smooth muscle cells have also been isolated from patient biopsies and cultured in vitro as a more controlled experimental system. However, in vitro approaches have focused primarily on measuring the effects of biochemical stimuli and neglected biomechanical stimuli, despite the extensive evidence indicating that remodeling of tissue rigidity or excessive strain is associated with uterine disorders. In this review, we first describe the existing approaches for modeling human myometrium with animal models and human tissue strips and compare their advantages and disadvantages. Next, we introduce existing in vitro techniques and assays for assessing contractility and summarize their applications in elucidating the role of biochemical or biomechanical stimuli on human myometrium. Finally, we conclude by proposing the translation of “organ on chip” approaches to myometrial smooth muscle cells as new paradigms for establishing their fundamental mechanobiology and to serve as next-generation platforms for drug development.
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Mehasseb, Mohamed K., S. C. Bell, and M. A. Habiba. "Neonatal administration of tamoxifen causes disruption of myometrial development but not adenomyosis in the C57/BL6J mouse." REPRODUCTION 139, no. 6 (June 2010): 1067–75. http://dx.doi.org/10.1530/rep-09-0443.
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We previously demonstrated that in the CD-1 mouse, which exhibits a high incidence of age-related adenomyosis, neonatal exposure to tamoxifen induced premature uterine adenomyosis and was associated with abnormal development particularly of the inner myometrium. In the present study, we examined the effect of neonatal tamoxifen administration upon uterine development in the C57/BL6J mouse strain that is not known to develop uterine adenomyosis. Female C57/BL6J pups (n=20) were treated with oral tamoxifen (1 mg/kg) from age 1 to 5 days. Uteri from control and treated mice were obtained on days 5, 10, 15 and 42 of age. We examined sections histologically using image analysis and immunohistochemistry for α-smooth muscle actin (ACTA2, α-SMA), desmin, vimentin, laminin, fibronectin and oestrogen receptor-α (ESR1). Following tamoxifen exposure, all uteri showed inner myometrium thinning, lack of continuity, disorganisation and bundling. However, adenomyosis was not seen in any uterus. ACTA2 immunostaining was less in the circular muscle layer of treated mice. The temporal pattern of desmin immunostaining found in control mice was absent in tamoxifen-treated mice. There was no difference in the localisation of laminin or fibronectin between control and tamoxifen-treated groups. However, laminin immunostaining was reduced in the circular muscle layer of treated mice. Vimentin could not be detected in either group. In conclusion, our results demonstrate that the development of the inner myometrium is particularly sensitive to oestrogen antagonism, and is affected by steroid receptor modulation. Although tamoxifen induces inner myometrial changes including that of ACTA2, desmin, ESR1 and laminin expression in C57/BL6J neonatal mice similar to those induced in CD-1 mice, C57/BL6J mice did not develop premature adenomyosis. Thus, disruption of the development and differentiation of the inner myometrium cannot alone explain the development of tamoxifen-associated adenomyosis, and this must be dependent upon its interaction with strain-dependent factors.
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Donoghue, J. F., F. L. Lederman, and P. A. W. Rogers. "285. Endometrial lymphatics are reduced in the functionalis compared to basalis and myometrium." Reproduction, Fertility and Development 17, no. 9 (2005): 120. http://dx.doi.org/10.1071/srb05abs285.
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Information on uterine lymphatics is limited. The aim of this study was to characterise uterine lymphatic vessels and the corresponding growth factors in the endometrium and myometrium across the normal human menstrual cycle. Uterine tissues were collected from patients undergoing hysterectomy. Lymphatic and microvascular density (MVD/mm2) was determined on serial sections of full thickness uterus (n = 45) with antibodies to D2-40, CD31, CD34 and FVIII. Lymphangiogenic growth factors VEGF-C and VEGF-D immunolocalisation was also determined on serial sections. VEGF-C, VEGF-D and lymphatic endothelial cell markers VEGF-R3 and D2-40 protein expression was determined on protein extracted from myometrium and endometrium and separated by SDS-PAGE from proliferative (n = 5) and secretory (n = 5) hysterectomy specimens. The lymphatic vessels were closely associated with smooth muscle cells of spiral arterioles and VEGF-C and VEGF-D were primarily localised in the endometrial glands, luminal epithelium and myometrial smooth muscle bundles. The lymphatic MVD was significantly reduced in the functionalis (15.1 ± 2.3mm2) compared to basalis (80 ± 11.4mm2) and myometrium (63 ± 9.2mm2). Overall, lymphatics constituted 12% of all vessels in the functionalis, 60 % in the basalis and 30% of the myometrium. D2-40 positive uterine lymphatics showed considerable heterogeneity, with 88% co-localisation with the blood vessel marker CD31, but only 46% expressing CD34 and 31% with FVIII. Protein expression of VEGF-C, VEGF-D, VEGF-R3 and D2-40 were significantly reduced during the proliferative phase compared to the secretory phase and were also significantly reduced in the endometrium compared to the myometrium across the cycle (P ≤ 0.05). Endometrial functionalis lymphatics are reduced in conjunction with a reduction in lymphangiogenic growth factors compared with the myometrium.
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Marinkin, I. O., D. A. Solyanikov, A. V. Volchek, E. S. Mikhailova, L. A. Piven, and S. V. Aidagulova. "Enzyme immunoassay of interleukin content in tumor supernatants in patients with multiple uterine myoma." Ural Medical Journal 20, no. 6 (March 23, 2022): 51–56. http://dx.doi.org/10.52420/2071-5943-2021-20-6-51-56.
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Introduction. Uterine leiomyoma is the most common benign tumor in women, which is accompanied by the life quality decrease and infertility. Despite numerous studies, the etiology of uterine myoma is still unknown.The aim of the study was to determine the effects of a mixture of polyclonal activators on the interleukin production by dominant myomatous and myometrial tissue samples under treating by ulipristal acetate (UA), a selective modulator of progesterone receptors.Materials and methods. Surgical material of 35 reproductiveaged women with multiple uterine myoma (1st group – without hormone therapy, 2nd group – after UA) was studied using enzyme immunoassay analysis. After determining of cytokine production, being spontaneous and stimulated by polyclonal activators phytohemagglutinin, concanavalin A, and lipopolysaccharide, the cytokine production stimulation index (SIPA) was calculated, followed by statistical analysis.Results. In patients of the 1st group the SIPA of IL-1β, IL-6 and IL-10 in the myomatous nodes and myometrium did not differ; at the same time, SIPA of IL-18 and 17-OH-progesterone were statistically higher in the myometrium samples than in the nodes (p < 0.05). In patients of the 2nd group, who have been treated by UA before myomectomy, there was a significantly higher SIPA of the IL-6 (p < 0.001) and IL-10 (p = 0.002) in the myometrium samples, compared with the dominant nodes. When comparing the nodes and myometrium between two groups, it was revealed that, compared with the 1st group, in patients using UA in the supernatants of myomatous nodes, out of 5 studied markers, the SIPA of the pro-inflammatory cytokine Il-6 was down-regulated (p = 0.013). In the myometrial supernatants in the 2nd group, there were a higher SIPA of anti-inflammatory IL-10 (p < 0.001), as well as the lower levels of pro-inflammatory IL-18 (p < 0.001).Discussion. The results of study demonstrate the anti-inflammatory effect of UA on the cellular elements of the dominant myomatous nodes and perifocal myometrium, and also confirm the role of inflammation in the pathogenesis of uterine fibroids.Conclusion. Polyclonal activators during in vitro incubation, had multidirectional effects on the production of some interleukins and the content of the progesterone metabolite in the tissue of the dominant myomatous node and perifocal myometrium.
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Korzekwa, A. J., M. Łupicka, B. M. Socha, and A. A. Szczepańska. "Estradiol Reduces Connexin43 Gap Junctions in the Uterus during Adenomyosis in Cows." Polish Journal of Veterinary Sciences 19, no. 3 (September 1, 2016): 609–17. http://dx.doi.org/10.1515/pjvs-2016-0076.
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Abstract Adenomyosis is defined as the presence of glandular foci external to the endometrium of the uterus, either in the myometrium or/and perimetrium, depending on the progress of this dysfunction. To date, we showed that steroids secretion and prolactin expression and proliferative processes are disturbed during uterine adenomyosis in cows. During endometriosis in eutopic endometrium in women, gap junctions are down regulated. The transmembrane gap junction protein, connexin (Cx43) is necessary for endometrial morphological, biochemical and angiogenic functions. The aim of this study is recognition of adenomyosis etiology by determination of the role of Cx43 in this process. Immunolocalization and comparison of Cx43 mRNA and protein expression in healthy (N=9) and adenomyotic uterine tissue (N=9), and Cx43 mRNA expression (real time PCR) in uterine stromal – myometrium co-culture under 24-hour stimulation with 17-beta estradiol (10−7M) isolated from healthy (N=5) and adenomyotic (N=5) cows were determined. Cx43 was localized in healthy and adenomyotic uteri. mRNA and protein expression was down-regulated in uterine tissue in adenomyotic compared with healthy cows (p<0.05). Estradiol stimulated Cx43 mRNA expression in myometrial cell culture and co-culture of stromal and myometrial cells in adenomyotic compared with healthy cows (p<0.05). In summary, down-regulation of Cx43 expression in the junction zone might play an important role in pathogenesis of adenomyosis. Estradiol modulates gap junctions during adenomyosis.
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Zhai, Junyu, Silvia Vannuccini, Felice Petraglia, and Linda C. Giudice. "Adenomyosis: Mechanisms and Pathogenesis." Seminars in Reproductive Medicine 38, no. 02/03 (May 2020): 129–43. http://dx.doi.org/10.1055/s-0040-1716687.
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AbstractAdenomyosis is a common disorder of the uterus, and is associated with an enlarged uterus, heavy menstrual bleeding (HMB), pelvic pain, and infertility. It is characterized by endometrial epithelial cells and stromal fibroblasts abnormally found in the myometrium where they elicit hyperplasia and hypertrophy of surrounding smooth muscle cells. While both the mechanistic processes and the pathogenesis of adenomyosis are uncertain, several theories have been put forward addressing how this disease develops. These include intrinsic or induced (1) microtrauma of the endometrial–myometrial interface; (2) enhanced invasion of endometrium into myometrium; (3) metaplasia of stem cells in myometrium; (4) infiltration of endometrial cells in retrograde menstrual effluent into the uterine wall from the serosal side; (5) induction of adenomyotic lesions by aberrant local steroid and pituitary hormones; and (6) abnormal uterine development in response to genetic and epigenetic modifications. Dysmenorrhea, HMB, and infertility are likely results of inflammation, neurogenesis, angiogenesis, and contractile abnormalities in the endometrial and myometrial components. Elucidating mechanisms underlying the pathogenesis of adenomyosis raise possibilities to develop targeted therapies to ameliorate symptoms beyond the current agents that are largely ineffective. Herein, we address these possible etiologies and data that support underlying mechanisms.
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Cramer, Stewart F., and Debra S. Heller. "A Review and Reconsideration of Nonneoplastic Myometrial Pathology." International Journal of Surgical Pathology 26, no. 2 (December 18, 2017): 104–19. http://dx.doi.org/10.1177/1066896917748194.
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From 1861 to 1962, clinicopathologic research tried to explain the association of abnormal uterine bleeding with uterine enlargement. The etiology was theorized as metropathy, suggesting that myometrial dysfunction may predispose to abnormal uterine bleeding. Research reached a nadir in 1962, when a major review dismissed myometrial hypertrophy as a plausible explanation after prior rejections of the theories of chronic myometritis, fibrosis uteri, and subinvolution as causes of bleeding. Subsequent to this arose a crusade against unnecessary hysterectomies in the 1970s. Although myometrial hyperplasia was proposed in 1868, it is only in the past 25 years that tangible evidence has supported that idea. It now appears that clinically enlarged uteri are due to globoid outward bulging of the uterus, caused by increased intramural pressure—often unrelated to either uterine weight or myometrial thickness. Abnormal (dysfunctional) uterine bleeding may often be due to spontaneous rupture of thrombosed dilated endometrial vessels, due to the combined effects of obstructed venous drainage by increased intramural pressure, and Virchow’s triad. Despite a century-old known association of parity with naturally occurring outer wall myometrial scars (fibrosis uteri with elastosis), it was not previously suggested that these may reflect healing reactions to muscle tears during labor and delivery. We now suggest that smaller, similar inner wall elastotic scars in the nerve-rich inner myometrium may explain many cases of pelvic pain. This review suggests that diverse pressure-related lesions may be present in clinically abnormal uteri that have been called “normal” since the crusade against unnecessary hysterectomy.
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Li, Shuanfang, Tung-Chin Chiang, Gloria R. Davis, Rachele M. Williams, Valerie P. Wilson, and John A. McLachlan. "Decreased Expression of Wnt7a mRNA Is Inversely Associated with the Expression of Estrogen Receptor-α in Human Uterine Leiomyoma." Journal of Clinical Endocrinology & Metabolism 86, no. 1 (January 1, 2001): 454–57. http://dx.doi.org/10.1210/jcem.86.1.7276.
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Wnt-7a gene not only guides the development of the anterior-posterior axis in the female reproductive tract, but also plays a critical role in uterine smooth muscle pattering and maintenance of adult uterine function. This gene is also responsive to changes in the levels of sex steroid hormone in the female reproductive tract. To explore the molecular mechanisms underlying the pathogenesis of uterine leiomyoma, the expression of Wnt7a mRNA in the leiomyoma has been assessed. RT-PCR was performed on uterine leiomyomas and the adjacent myometria. Of 30 cases of leiomyomas studied, 67% showed a decreased mRNA level as compared to the paired myometria. On the other hand, estrogen receptor-α (ER-α) mRNA is hyper-expressed in 67% of the leiomyomas as compared to their paired myometrium. An inverse association at mRNA expression was found between Wnt7a and ER-α. Miller et alhas shown that fetal exposure of DES results in de-regulation of Wnt7a during uterine morphogenesis. Referring to their results, we have postulated that hypersensitivity of leiomyoma cells to estrogen may deregulate the Wnt7a expression. Decreased expression of Wnt7a may lead to loss of control in patterning of the myometrium and result in development of leiomyoma
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Jana, Barbara, Joanna Czarzasta, and Jerzy Jaroszewski. "Synthesis of leukotrienes in porcine uteri with endometritis induced by infection with Escherichia coli." Reproduction, Fertility and Development 26, no. 7 (2014): 1007. http://dx.doi.org/10.1071/rd13191.
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Leukotrienes (LTs) are lipid mediators that play a significant role in the inflammatory process. Their production in inflamed uteri is not fully understood. The present experiment aimed to determine LTB4 and LTC4 amounts, 5-lipooxygenase (5-LO), LTA4 hydrolase (LTAH) and LTC4 synthase (LTCS) mRNA levels and protein expression in inflamed porcine uteri. On Day 3 of the oestrous cycle (Day 0 of the study), either Escherichia coli suspension or saline were infused into uterine horns. Collection of uterine tissues and washings took place eight or sixteen days later. In gilts suffering from endometritis increased LTB4 and LTC4 levels in the endometrium and washings and 5-LO mRNA levels in the myometrium on Days 8 and 16, 5-LO protein levels in the endometrium and myometrium on Day 8, LTAH mRNA and protein levels in the endometrium and myometrium on Days 8 and 16, respectively. Although LTCS mRNA and protein expression in the myometrium and LTCS protein expression in the endometrium were enhanced on Day 16 after Escherichia coli inoculation, LTCS mRNA levels decreased on Day 8 in both tissues. Our study shows the upregulation of LT production in inflamed porcine uteri, which suggests the importance of these factors to the process of uterine inflammation.
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Word, R. A., M. L. Casey, K. E. Kamm, and J. T. Stull. "Effects of cGMP on [Ca2+]i, myosin light chain phosphorylation, and contraction in human myometrium." American Journal of Physiology-Cell Physiology 260, no. 4 (April 1, 1991): C861—C867. http://dx.doi.org/10.1152/ajpcell.1991.260.4.c861.
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Adenosine 3',5'-cyclic monophosphate (cAMP) is believed to be an important mediator of myometrial relaxation, and there is evidence to suggest that guanosine 3',5'-cyclic monophosphate (cGMP) is a mediator of smooth muscle relaxation in vascular and probably nonvascular tissues. To investigate the biochemical mechanisms involved in regulation of human myometrial contractility, we studied the effects of analogues of cAMP and cGMP, as well as activators of adenylate and guanylate cyclases, on uterine smooth muscle contractile activity. We found that myometrial smooth muscle cells in culture respond to analogues of cGMP and cAMP, as well as activators of guanylate cyclase, with a significant decrease in the resting and endothelin-induced increase in [Ca2+]i. Treatment of human uterine smooth muscle strips with sodium nitroprusside or isoproterenol results in diminished force and frequency of contraction as well as a decrease in the rate and extent of myosin light chain phosphorylation in spontaneous contractions of human myometrium. cGMP did not effect relaxation of endothelin-stimulated contractions of human myometrium, but the relaxation effects of cGMP were dramatic in precontracted bovine tracheal and human fetal aortic smooth muscles. Whereas cGMP and cAMP act to promote a decrease in the force and frequency of spontaneous contractions in human myometrium, this tissue is not as responsive to the actions of cyclic nucleotides as are other types of smooth muscle.
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Maiti, K., J. W. Paul, M. Read, E. C. Chan, S. C. Riley, P. Nahar, and R. Smith. "G-1-Activated Membrane Estrogen Receptors Mediate Increased Contractility of the Human Myometrium." Endocrinology 152, no. 6 (March 22, 2011): 2448–55. http://dx.doi.org/10.1210/en.2010-0979.
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Estrogens are key mediators of increased uterine contractility at labor. We sought to determine whether membrane-associated estrogen receptors, such as the recently described seven-transmembrane receptor G protein-coupled receptor 30 (GPR30), mediated some of this effect. Using human myometrium obtained at term cesarean section before or after the onset of labor, we demonstrated the presence of GPR30 mRNA and protein using quantitative RT-PCR and Western blotting. GPR30 receptor was localized to the cell membrane and often colocalized with calveolin-1. Using the specific estrogen membrane receptor agonist G-1 and myometrial explants, we showed that membrane receptor activation led to phosphorylation of MAPK and the actin-modifying small heat shock protein 27. Using myometrial strips incubated with G-1 or vehicle we demonstrated that estrogen membrane receptor activation increased the myometrial contractile response to oxytocin. These data suggest that activation of the plasma membrane estrogen receptor GPR30 likely participates in the physiology of the human myometrium during pregnancy and identifies it as a potential target to modify uterine activity.
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Jana, Barbara, Jerzy Jaroszewski, Jan Kucharski, Marlena Koszykowska, Jolanta Górska, and Włodzimierz Markiewicz. "Participation of Prostaglandin E2 in Contractile Activity of Inflamed Porcine Uterus." Acta Veterinaria Brno 79, no. 2 (2010): 249–59. http://dx.doi.org/10.2754/avb201079020249.
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The aim of our study was to estimate the participation of prostaglandin E2 (PGE2) in the contractile activity of inflamed porcine uterus. On day 3 of the oestrous cycle, 50 ml of saline or 50 ml of Escherichia coli suspension, containing 109 colony-forming units/ml, was injected into each uterine horn in the control or experimental group, respectively. Seven days later the uteri were collected. Endometritis developed in all bacteria-inoculated gilts. Endometrium/myometrium and myometrium strips were incubated with PGE2 alone or together with PGE2 receptor (EP) subtypes (EP2, EP4, EP1 and EP3) blockers: AH 6809 (BEP2), ONO-AE2 (BEP4), ONO-AE3-240 (BEP1) and SC19220 (BEP3), respectively. In the control group, PGE2 (10-8 and 10-7 M) increased the intensity of contractions in endometrium/myometrium, and at the higher dose in myometrium. PGE2 (10-8 M) decreased the contraction intensity of the strips from inflamed uteri. After the use of BEP2, PGE2 (10-7 M) increased the values of this indicator in endometrium/myometrium and myometrium from the control gilts. In these animals, PGE2 (10-8 M) in the presence of BEP4 reduced the contraction intensity in endometrium/myometrium. In the bacterial group, PGE2 (10-8 M) in the presence of BEP2 and BEP4 enhanced the intensity of contractions in myometrium. Similar reaction was evoked by PGE2 (10-7 M) in endometrium/myometrium of the inflamed uteri in the presence of BEP4. The intensity of contractions in myometrium from the inflamed uteri significantly decreased after the use of BEP1 and PGE2 (10-7 M). PGE2 (10-7 M) administered after BEP3, significantly decreased the intensity of contractions in myometrium of the control gilts. These results show that PGE2 decreases the contraction intensity of inflamed porcine uteri. Further studies are needed to closely determine the role of PGE2 and other prostanoids in the contractile activity of inflamed uterine tissue.
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Shynlova, Oksana, Ruth Kwong, and Stephen J. Lye. "Mechanical stretch regulates hypertrophic phenotype of the myometrium during pregnancy." REPRODUCTION 139, no. 1 (January 2010): 247–53. http://dx.doi.org/10.1530/rep-09-0260.
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The adaptive growth of the uterus is a critical event that involves changes in cellular phenotypes throughout pregnancy. In early pregnancy, uterine growth is due to hyperplasia of uterine smooth muscle cells (SMCs) within the myometrium; however, the major component of myometrial growth occurs after mid-gestation. This study sought to test the hypothesis that increase in myometrial growth seen during late pregnancy is due to SMC hypertrophy caused by mechanical stretch of uterine tissue by a growing fetus(es) by providing direct measurements of individual SMC size. We employed a stereological approach to calculate the average cell volumes of uterine myocytes through diameter measurements using the Stereoinvestigator statistical software. Uterine tissues were collected from nonpregnant Wistar rats, as well as from gravid and nongravid horns of unilaterally pregnant animals on gestational days (d) 8 (early gestation), 14 (mid-gestation), 19 (late gestation), 22 (term), and 4 dayspost partum. Anti-caveolin-1 immunostaining was used to clearly delineate SMC boundaries. The stereological analysis revealed that the dramatic increase in myometrial growth seen during late gestation (d19–22) is due to a threefold increase in the size of uterine myocytes. A significant increase in SMC volumes was detected in the gravid uterine horn as compared with the corresponding empty horn of unilateral term pregnant animals (day 22, mean cell volume 1114 vs 361 μm3,P<0.05), indicating the effect of uterine occupancy. The restriction of the hypertrophy to cells within the gravid horn suggests that it may be a response to the biological mechanical stretch of uterine walls by the growing fetus(es) and placenta(s).
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You, Xingji, Zixi Chen, Huina Zhao, Chen Xu, Weina Liu, Qianqian Sun, Ping He, Hang Gu, and Xin Ni. "Endogenous hydrogen sulfide contributes to uterine quiescence during pregnancy." Reproduction 153, no. 5 (May 2017): 535–43. http://dx.doi.org/10.1530/rep-16-0549.
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Recent evidence suggests that uterine activation for labor is associated with inflammation within uterine tissues. Hydrogen sulfide (H2S) plays a critical role in inflammatory responses in various tissues. Our previous study has shown that human myometrium produces H2S via its generating enzymes cystathionine-γ-lyase (CSE) and cystathionine-β-synthetase (CBS) during pregnancy. We therefore explored whether H2S plays a role in the maintenance of uterine quiescence during pregnancy. Human myometrial biopsies were obtained from pregnant women at term. Uterine smooth muscle cells (UMSCs) isolated from myometrial tissues were treated with various reagents including H2S. The protein expression of CSE, CBS and contraction-associated proteins (CAPs) including connexin 43, oxytocin receptor and prostaglandin F2αreceptor determined by Western blot. The levels of cytokines were measured by ELISA. The results showed that CSE and CBS expression inversely correlated to the levels of CAPs and activated NF-κB in pregnant myometrial tissues. H2S inhibited the expression of CAPs, NF-κB activation and the production of interleukin (IL)-1β, IL-6 and tumor necrosis factor α (TNFα) in cultured USMCs. IL-1β treatment reversed H2S inhibition of CAPs. Knockdown of CSE and CBS prevented H2S suppression of inflammation. H2S modulation of inflammation is through KATPchannels and phosphoinositide 3-kinase (PI3K) and extracellular signal-regulated kinase (ERK) signaling pathways. H2S activation of PI3K and ERK signaling is dependent on KATPchannels. Our data suggest that H2S suppresses the expression of CAPs via inhibition of inflammation in myometrium. Endogenous H2S is one of the key factors in maintenance of uterine quiescence during pregnancy.
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Young, R. C. "Myocytes, myometrium and uterine contractions." Journal of Biomechanics 39 (January 2006): S341. http://dx.doi.org/10.1016/s0021-9290(06)84352-6.
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YOUNG, R. C. "Myocytes, Myometrium, and Uterine Contractions." Annals of the New York Academy of Sciences 1101, no. 1 (February 15, 2007): 72–84. http://dx.doi.org/10.1196/annals.1389.038.
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Frühauf, Filip, Michal Zikan, Ivana Semeradova, Pavel Dundr, Kristyna Nemejcova, Ladislav Dusek, David Cibula, and Daniela Fischerova. "The Diagnostic Accuracy of Ultrasound in Assessment of Myometrial Invasion in Endometrial Cancer: Subjective Assessment versus Objective Techniques." BioMed Research International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/1318203.
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The aim of this study was to assess the diagnostic accuracy of subjective ultrasound evaluation of myometrial invasion of endometrial cancer and to compare its accuracy to objective methods. All consecutive patients with histologically proven endometrial cancer, who underwent ultrasound evaluation followed by surgical staging between January 2009 and December 2011, were prospectively enrolled. Myometrial invasion was evaluated by subjective assessment using ultrasound (<50% or ≥50%) and calculated as deepest invasion/normal myometrium ratio (Gordon’s ratio) and as tumor/uterine anteroposterior diameter ratio (Karlsson’s ratio). Histological assessment from hysterectomy was considered the gold standard. Altogether 210 patients were prospectively included. Subjective assessment and two objective ratios were found to be statistically significant predictors of the myometrial invasion (AUC = 0.65, p value < 0.001). Subjective assessment was confirmed as the most reliable method to assess myometrial invasion (79.3% sensitivity, 73.2% specificity, and 75.7% overall accuracy). Deepest invasion/normal myometrium (Gordon’s) ratio (cut-off 0.5) reached 69.6% sensitivity, 65.9% specificity, and 67.3% overall accuracy. Tumor/uterine anteroposterior diameter (Karlsson’s) ratio with the same cut-off reached 56.3% sensitivity, 76.4% specificity, and 68.1% overall accuracy. The subjective ultrasound evaluation of myometrial invasion performed better than objective methods in nearly all measures but showed statistically significantly better outcomes only in case of sensitivity.
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Price, SA, I. Pochun, S. Phaneuf, and A. Lopez Bernal. "Adenylyl cyclase isoforms in pregnant and non-pregnant human myometrium." Journal of Endocrinology 164, no. 1 (January 1, 2000): 21–30. http://dx.doi.org/10.1677/joe.0.1640021.
Full textAbstract:
The precise factors involved in the transition of the relaxed pregnant uterus to the contractile state at the onset of parturition remain unclear, but it is accepted that cAMP-generating pathways contribute to uterine relaxation. We have previously reported an increased expression of the adenylyl cyclase (AC)-stimulating protein Galphas in human myometrium during gestation, with a corresponding increase in GTP-stimulated AC activity. However, little is known about the predominating AC isoforms expressed during pregnancy. This information is important, because although all AC isoforms are stimulated by Galphas, their regulation by other signalling molecules is very different. In the present study we have identified the isoforms of AC expressed in both pregnant and non-pregnant myometrium by mRNA analysis and immunoblotting. mRNA encoding for AC I, II, III, VIII and IX was present in non-pregnant and pregnant myometrium, and in cultured myometrial cells. Differing levels of AC protein could be detected in myometrial plasma membranes, with decreased levels of Group 1 (isoforms I, III and VIII) and Group 4 (IX) ACs allied with increased levels of Group 2 (II, IV and VII) and 3 (V and VI) ACs during pregnancy. These findings imply a role for Group 2-activating pathways, e.g. G-protein betagamma-subunits and protein kinase C, in the maintenance of uterine quiescence, whilst suggesting a lesser involvement of calcium-calmodulin complex, an activator of Group 1 AC isoforms, in uterine relaxation during gestation. These data may provide an alternative pharmacological approach for the attenuation of preterm labour.
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Chapman, Neil R., G. Nicholas Europe-Finner, and Stephen C. Robson. "Expression and Deoxyribonucleic Acid-Binding Activity of the Nuclear Factor κB Family in the Human Myometrium during Pregnancy and Labor." Journal of Clinical Endocrinology & Metabolism 89, no. 11 (November 1, 2004): 5683–93. http://dx.doi.org/10.1210/jc.2004-0873.
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Abstract In humans, the factors that govern the switch from myometrial quiescence to coordinated contractions at the initiation of labor are not well defined. The onset of parturition is itself associated with increases in a number of proinflammatory factors, many of which are regulated by the nuclear factor κB (NF-κB) family of transcription factors. The expression and DNA-binding activity of NF-κB in the myometrium during gestation and parturition were examined. Levels of c-Rel, p50, and p105 NF-κB species were dramatically reduced in pregnant myometrium compared with nonpregnant (NP) controls, whereas expression of the RelA subunit remained uniform. Importantly, during labor, expression of all subunits was observed to be significantly reduced in all myometrial samples studied relative to NP levels. Moreover, for RelA, c-Rel, and p50 subunits, there was a gradient of expression between laboring upper (corpus) and lower uterine segment myometrium. No RelB or p52 subunits could be detected. EMSAs identified changes in NF-κB subunit composition in the myometrium during pregnancy and labor, with p50 homodimers predominant in NP tissues being replaced with RelA:p50 heterodimers in pregnant and laboring samples. Significantly, RelA was observed to be phosphorylated at serine-536, implicating the involvement of the phosphatidylinositol-3-kinase/AKT pathway in NF-κB function in the myometrium.
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Sharmazanova, Olena, Inessa Safonova, and Yulia Mityakova. "The importance of compression sonoelastography in improving the diagnostics of the pathology of myometrium." EUREKA: Health Sciences, no. 4 (July 30, 2021): 65–72. http://dx.doi.org/10.21303/2504-5679.2021.001908.
Full textAbstract:
The diversity of the clinical picture and the asymptomatic nature of the clinical manifestations of myometrial pathology cause difficulties in diagnosis. There is a lack of reliable diagnostic criteria for this pathology, in particular, imaging, especially with the simultaneous combination of adenomyosis and leiomyoma.
The aim of the research. Determination of the possibility of compression sonoelastography in the diagnosis of myometrial pathology and determination of its sonoelastography characteristics in leiomyoma and adenomyosis, as well as comparison of sonoelastography results with histological data.
Materials and methods. Elastography images of 155 patients with adenomyosis and leiomyoma, as well as combined pathology, were analyzed, the elastography diagnosis of which was confirmed by histological examination.
Results. Leiomyoma and adenomyosis had different elastography characteristics (strain ratios) with different color mapping; their specific characteristics and main differences are determined. Based on sonoelastography, the majority of patients (n=30) were suspected of having uterine fibroids, 14 had adenomyosis, and 42 had adenomyosis and fibroids. Sonoelastography revealed histological signs of adenomyosis in 3 patients with uterine leiomyoma.
Conclusions. Ultrasound examination using compression sonoelastography in such pathological conditions of the myometrium as adenomyosis and leiomyoma, as well as unchanged myometrium, makes it possible to determine changes in the degree of elasticity of the myometrium in the corresponding pathology. Sonoelastography allows the identification of clear distinguishing features of fibroids and adenomyosis. The unchanged myometrium has a certain elasticity, which can be equated to a specific numerical value – the coefficient of deformation. This indicator has different meanings in myoma and adenomyosis, which makes it possible to differentiate these pathological conditions of the myometrium. Compression sonoelastography is able to identify clear distinguishing features of leiomyoma and adenomyosis, and consistency of diagnoses based on sonoelastography and histology is significant but not optimal.
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Maruyama, Tetsuo, Hirotaka Masuda, Masanori Ono, Takashi Kajitani, and Yasunori Yoshimura. "Human uterine stem/progenitor cells: their possible role in uterine physiology and pathology." REPRODUCTION 140, no. 1 (July 2010): 11–22. http://dx.doi.org/10.1530/rep-09-0438.
Full textAbstract:
The human uterus mainly consists of the endometrium and the outer smooth muscle layer termed the myometrium. The uterus harbours the exceptional and remarkable regenerative ability responsible for cyclical regeneration and remodelling throughout the reproductive life. The uterus must swiftly and cooperatively enlarge to hold the growing foetus during pregnancy. Furthermore, the endometrium, in particular the functionalis layer, must also regenerate, differentiate and regress with each menstrual cycle under hormonal control. Endometrial regeneration from the basal layer is thought to contribute to replacement of the functionalis layer followed by its slough off during menses and parturition. These morphological and functional features of human endometrium can be reproduced in murine models in which severely immunodeficient mice are xenotransplanted with dispersed human endometrial cells under the kidney capsule. The uterine myometrium possesses the similar plasticity of the endometrium. This is demonstrated by multiple cycles of pregnancy-induced enlargement and regression after parturition. It is likely that regeneration and remodelling in the female reproductive tract are achieved presumably through endometrial and myometrial stem cell systems. Recent evidence now supports the existence of these stem cell systems in humans. Here, we will review our current understanding of uterine stem/progenitor cells. We also propose a novel hypothetical model in which stem cell activities explain the physiological remodelling and regeneration of the human uterus and the pathogenesis of gynaecological diseases such as endometriosis.
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Van Quynh Duong, Thu, Alexandra Yaw, Duong Nguyen, and Hanne Mette Hoffmann. "The Circadian Clock Gene Bmal1 Modulates Myometrium Contractile Function in Pregnant Mice." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A754—A755. http://dx.doi.org/10.1210/jendso/bvab048.1534.
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Abstract Caesarian section should be avoided unless medically required. Caesarian section is often a result of failed labor enhancement. While most natural births occur at night, labor enhancement is often scheduled during the day. We propose that the disparity between the commonly used timing of labor enhancement in the clinic, from the timing of natural birth, could contribute to the high rate of labor induction failure. Oxytocin receptor agonists are the most used labor enhancing agents. In pregnant non-human primates, oxytocin enhances uterine contractions more efficiently at night than during the day, suggesting a daily change in uterine sensitivity to oxytocin in pregnancy. To identify the molecular mechanisms generating daily changes in uterine function, we here explore the role of the molecular clock gene, Bmal1 (Brain and muscle ARNTL1-like), in the pregnant mouse myometrium. BMAL1 is a transcription factor required to generated circadian rhythms at the cellular level. We hypothesize that Bmal1 in uterine myometrial cells generates circadian rhythms and establishes the daily change in uterine contractile response to oxytocin. To evaluate circadian rhythms ex vivo, we collected myometrium samples from the validated circadian Per2:luciferase reporter mice at gestation day 17-18. We found that the pregnant mouse myometrium possesses circadian rhythms, which are generated by the molecular clock, as triple transgenic Per2:luciferase mice with Bmal1 conditionally deleted in the myometrium (cKO) do not have rhythmic expression of the Per2:luciferase reporter. To determine if BMAL1 is required to establish uterine contractions, we used a myograph to measure ex vivo uterine contractions at gestation day 17-18. In controls, uterine contraction force was significantly higher at ZT15 (3h after lights OFF) versus ZT3 (3h after lights ON). Interestingly, our preliminary data show increased basal contractile force at ZT15 in cKO as compared to controls. In addition, the cKO uterus contracted stronger to oxytocin than controls. Our findings identify Bmal1 as a clock gene modulating basal contractions in the mouse uterus and indicate Bmal1 might be a regulator of uterine sensitivity to oxytocin. Future work will focus on identifying the molecular mechanisms driven by BMAL1 to regulate uterine function in pregnancy. This work has the potential to provide insights into how we can improve labor enhancing treatment strategies in the clinic in the future.
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Engstrom, T., P. Bratholm, H. Vilhardt, and NJ Christensen. "Beta2-adrenoceptor desensitization in non-pregnant estrogen-primed rat myometrium involves modulation of oxytocin receptor gene expression." Journal of Molecular Endocrinology 20, no. 2 (April 1, 1998): 261–70. http://dx.doi.org/10.1677/jme.0.0200261.
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The nona-peptide oxytocin (OT) induces contraction of the myometrium by interaction with specific plasma membrane associated OT receptors (OTR), whereas stimulation of beta2-adrenoceptors (beta2AR) causes relaxation. Homologous desensitization of the myometrium to both hormones has been described. However, a possible interaction between the two systems has not been investigated. In the present study, long-term in vivo treatment of non-pregnant estrogen-primed rats with isoproterenol decreased maximal relaxation of isolated uterine strips challenged with isoproterenol. Increased EC50 values of similarly treated animals suggest that the coupling between receptor occupancy and contractile response was impaired. Since beta2AR mRNA levels were left unchanged, we conclude that the homologous desensitization to beta2 stimulation is not due to changes in beta2AR gene expression. OT infusion did not alter beta2AR mRNA levels or isoproterenol-induced relaxation of isolated uterine strips. Treatment with OT had no effect on the amount of myometrial OTR mRNA. We have previously found that OT down-regulates OTR in the non-pregnant rat myometrium, but this therefore does not appear to take place at the level of mRNA production. Isoproterenol treatment resulted in a three-fold increase in OTR mRNA. This was accompanied by a 91% rise in OTR binding and an augmented contractile response of isolated uterine strips to OT, suggesting that the increased production of mRNA reflects formation of active receptors. Neither OTR affinity nor EC50 of in vitro strips was affected by isoproterenol treatment. We conclude that stimulation of beta2AR causes heterologous up-regulation of OTR in the non-pregnant estrogen-primed rat myometrium.
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Stevens, M. Yvette, John R. G. Challis, and Stephen J. Lye. "Corticotropin-Releasing Hormone Receptor Subtype 1 Is Significantly Up-Regulated at the Time of Labor in the Human Myometrium1." Journal of Clinical Endocrinology & Metabolism 83, no. 11 (November 1, 1998): 4107–15. http://dx.doi.org/10.1210/jcem.83.11.5272.
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Circulating concentrations of CRH rise late in human pregnancy, reaching a peak at labor. The presence of functional CRH receptors, CRH-R1 and CRH-R2, in the human myometrium suggests that CRH may modulate uterine activity. We hypothesized that the number of CRH receptors would be higher in myometrium than fetal membranes (FM) and would change during labor. Myometrial samples were collected from the lower segment (LS) in nonpregnant, preterm (32 ± 2 weeks), and term (39 ± 1.6 weeks) pregnant patients before and at labor. Fundus and LS samples were also collected from nonpregnant, pregnant, laboring, and postpartum women. FM were collected at term and at labor. We identified CRH receptors in myometrium and FM by semiquantitative RT-PCR and immunohistochemistry. CRH-R1 messenger ribonucleic acid (mRNA) in the LS was decreased in pregnancy and increased significantly in both preterm and term labor (P < 0.05), but remained unchanged in the fundus. CRH-R2 mRNA was present in 28% of LS myometrium with no change at labor. CRH-R1 and CRH-R2 protein was localized to myometrial smooth muscle in nonpregnant and laboring patients, with lower levels at term. CRH-R1 mRNA was present in chorion and decidua, but CRH-R2 was undetectable in these tissues. We conclude that CRH-R1 is expressed preferentially in myometrium and FM. Changes in CRH receptors during labor are consistent with CRH mediating effects on myometrial activity.
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Kousides, M., ME Story, JN Pennefather, SP Ziccone, and AW Ross. "Inhibitory potency of isoprenaline on guinea-pig and gravid human myometrium following extraneuronal uptake blockade." Reproduction, Fertility and Development 7, no. 1 (1995): 59. http://dx.doi.org/10.1071/rd9950059.
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The hypothesis that inhibitory effects of isoprenaline on myometrial contractility may be constrained by activation of putative intracellular beta-adrenoceptors negatively-coupled to adenylate cyclase was examined. Field-stimulated preparations of guinea-pig and human myometrium were used to examine the influence of the catecholamine extraneuronal uptake2 inhibitors, corticosterone and beta-oestradiol, on the inhibitory effects of the beta-adrenoceptor agonist, isoprenaline, on uterine contraction. Longitudinal and circular myometrial layers were obtained from guinea-pigs in dioestrus, primed with oestrogen before progesterone, or pregnant (Days 62-65). In the guinea-pig myometrium, corticosterone (30 microM) did not affect responses to isoprenaline. beta-oestradiol (10 microM) induced a small potentiation of the effects of isoprenaline on longitudinal myometrium from dioestrus guinea-pigs. Myometrial preparations were obtained from pregnant women (36-40 weeks gestation) undergoing caesarean section. Isoprenaline inhibited stimulation-evoked contractions in 7 of 10 preparations of the inner myometrial layer and in 5 of 8 preparations of outer myometrial layer. Corticosterone (30 microM) reduced the effects of isoprenaline on the inner layer and did not affect the outer layer. These results do not support the existence of mechanism involving isoprenaline-sensitive intracellular receptors which constrain responses to beta-adrenoceptor agonists.
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B.N, Gayathri, Mallikarjun A. Pattanashetti, and Priyadarshini M.M. "Histopathological Study of Myometrial Lesions of Uterus in a Tertiary Care Hospital of South India." Journal of Evidence Based Medicine and Healthcare 8, no. 06 (February 8, 2021): 293–97. http://dx.doi.org/10.18410/jebmh/2021/57.
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BACKGROUND The most commonly done gynaecological surgery worldwide is hysterectomy. Myometrial lesions contribute to majority of cases with abnormal uterine bleeding. Leiomyoma and adenomyosis are most common lesions seen in the myometrium. The present study was undertaken to identify the various types of myometrial pathologies in hysterectomy samples. METHODS This is a two-year retrospective cross-sectional study done from January 2017 to December 2018, in the Department of Pathology, Kodagu Institute of Medical Sciences, Madikeri. All the patients who underwent hysterectomy and myomectomy for myometrial lesions of uterus were included in the study. Hysterectomy specimens showing secondaries, gross infection, massive haemorrhage and necrosis were excluded from the study. Gross appearance and microscopic pathology were noted and results were analysed. RESULTS In this study, 148 specimens were included. Age range was from 20 years to 65 years. Histopathological examination revealed that 58.25 % of myometrial lesions were present in the age group of 41 to 50 years followed by age group of 31 to 40 years. Histopathological examination done showed the following diagnosis in patients - leiomyoma (85.13 %), adenomyosis (8.79 %) and leiomyoma with adenomyosis (6.08 %). CONCLUSIONS The commonest histopathological lesion in myometrium was leiomyoma (85.13 %) followed by adenomyosis (8.79 %). It is mandatory to examine the hysterectomy specimens adequately to diagnose myometrial lesions. KEYWORDS Myometrium, Leiomyoma, Adenomyosis
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Engstrom, T. "The regulation by ovarian steroids of prostaglandin synthesis and prostaglandin-induced contractility in non-pregnant rat myometrium. Modulating effects of isoproterenol." Journal of Endocrinology 169, no. 1 (April 1, 2001): 33–41. http://dx.doi.org/10.1677/joe.0.1690033.
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The objectives of the present study were to investigate the effects of the reproductive steroids oestradiol and progesterone on myometrial levels of cyclooxygenase-2 (COX-2) mRNA and PGF(2alpha) induced myometrial contractility and to study whether the effect of beta(2)-adrenoceptor stimulation by isoproterenol on the myometrium alters these parameters. Oestrogen treatment of ovariectomized rats increased myometrial COX-2 mRNA whereas PGF(2alpha) receptor (PGF(2alpha)-R) mRNA was unchanged following this treatment and maximal contractility (E(max)) of isolated uterine strips challenged with PGF(2alpha) was unaltered. Progesterone treatment alone decreased COX-2 mRNA in comparison with values obtained from oestrogen-treated animals, and in combination with oestrogen the enhancing effect of progesterone on COX-2 mRNA was curbed. EC(50) of uterine strips challenged with PGF(2alpha) increased following oestrogen treatment whereas this parameter was substantially decreased following progesterone treatment. When oestrogen was combined with isoproterenol infusion mRNA values of both COX-2 and PGF(2alpha)-R were reduced. Finally, when isoproterenol infusions were given in combination with both oestrogen and progesterone, PGF(2alpha)-R mRNA and E(max )were enhanced as compared with similar rats not having received isoproterenol. We conclude that oestrogen increases COX-2 mRNA production and subsequent prostaglandin synthesis in non-pregnant rat myometrium. We further conclude that in the oestrogen-dominated rat myometrium the relaxing effect of beta(2)-adrenoceptor stimulation involves attenuation of both prostaglandin synthesis and PGF(2alpha)-R expression. We finally conclude that in the presence of both oestrogen and progesterone this effect of beta(2)-adrenoceptor stimulation is restrained.
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Tica, Andrei A., Erica C. Dun, Oana S. Tica, Xin Gao, Jeffrey B. Arterburn, G. Cristina Brailoiu, Tudor I. Oprea, and Eugen Brailoiu. "G protein-coupled estrogen receptor 1-mediated effects in the rat myometrium." American Journal of Physiology-Cell Physiology 301, no. 5 (November 2011): C1262—C1269. http://dx.doi.org/10.1152/ajpcell.00501.2010.
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G protein-coupled estrogen receptor 1 (GPER), also named GPR30, has been previously identified in the female reproductive system. In this study, GPER expression was found in the female rat myometrium by reverse transcriptase-polymerase chain reaction and immunocytochemistry. Using GPER-selective ligands, we assessed the effects of the GPER activation on resting membrane potential and cytosolic Ca2+ concentration ([Ca2+]i) in rat myometrial cells, as well as on contractility of rat uterine strips. G-1, a specific GPER agonist, induced a concentration-dependent depolarization and increase in [Ca2+]i in myometrial cells. The depolarization was abolished in Na+-free saline. G-1-induced [Ca2+]i increase was markedly decreased by nifedipine, a L-type Ca2+ channel blocker, by Ca2+-free or Na+-free saline. Intracellular administration of G-1 produced a faster and transitory increase in [Ca2+]i, with a higher amplitude than that induced by extracellular application, supporting an intracellular localization of the functional GPER in myometrial cells. Depletion of internal Ca2+ stores with thapsigargin produced a robust store-activated Ca2+ entry; the Ca2+ response to G-1 was similar to the constitutive Ca2+ entry and did not seem to involve store-operated Ca2+ entry. In rat uterine strips, administration of G-1 increased the frequency and amplitude of contractions and the area under the contractility curve. The effects of G-1 on membrane potential, [Ca2+]i, and uterine contractility were prevented by pretreatment with G-15, a GPER antagonist, further supporting the involvement of GPER in these responses. Taken together, our results indicate that GPER is expressed and functional in rat myometrium. GPER activation produces depolarization, elevates [Ca2+]i and increases contractility in myometrial cells.
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Maggi, M., G. B. Vannelli, A. Peri, M. L. Brandi, G. Fantoni, S. Giannini, C. Torrisi, et al. "Immunolocalization, binding, and biological activity of endothelin in rabbit uterus: effect of ovarian steroids." American Journal of Physiology-Endocrinology and Metabolism 260, no. 2 (February 1, 1991): E292—E305. http://dx.doi.org/10.1152/ajpendo.1991.260.2.e292.
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Specific immunostaining for endothelin 1 (ET-1) was observed in the endometrium but not myometrium of rabbits. The staining was dramatically affected by subacute treatment with ovarian steroids: epithelial cells were predominantly positive in immature rabbits, whereas, in sex steroid-primed rabbits, ET-1 was mainly localized in the stromal compartment. Binding studies were performed in myometrium of estrogen-treated rabbits using labeled ET-1 and ET-3, the corresponding unlabeled peptides, and sarafotoxin b (SRTX). Mathematical modeling of experimental results indicates that two populations of sites are present in myometrium. One site (R1 = 1 pmol/mg protein) shows approximately the same affinity for ET-1, ET-3, and SRTX [dissociation constant (Kd) 100 pM], whereas the second site (R2 = 10 pmol/mg protein) selectively binds ET-1 (Kd 400 pM). According to binding studies, ET-1 was more potent than SRTX in stimulating uterine contraction "in vitro." The subacute administration of increasing concentrations of 17 beta-estradiol (0.2-200 micrograms/kg for 4 days), but not 17 beta-estradiol (200 micrograms/kg for 4 days) plus progesterone (5 mg/kg for 4 days), stimulates a dose-dependent increase in endothelin receptors in myometrium (half-maximal effective dose = 0.7 micrograms/kg for 4 days). However, estrogen treatment does not affect the concentration of endothelin receptors in myometrial cells in primary culture. Conversely, divalent ions like calcium and magnesium enhance the binding of ET-1 to both uterine membranes and cells. Our results indicate that in rabbit uterus endothelin is present in the endometrium, whereas specific receptors are located in myometrium.
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Riemer, R. K., C. Buscher, R. K. Bansal, S. M. Black, Y. He, and E. S. Natuzzi. "Increased expression of nitric oxide synthase in the myometrium of the pregnant rat uterus." American Journal of Physiology-Endocrinology and Metabolism 272, no. 6 (June 1, 1997): E1008—E1015. http://dx.doi.org/10.1152/ajpendo.1997.272.6.e1008.
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Nitric oxide (NO) relaxes uterine smooth muscle and is produced by the pregnant uterus. Our previous studies revealed an increase in rat uterine NO synthase (NOS) activity in pregnancy and a decline at term. In the present study, we have examined the distribution of NOS isoform expression to determine whether their regulation is consistent with a role in the inhibition of uterine contractions before term. At day 17-18 of pregnancy, NOS immunohistochemistry revealed expression of two isoforms: endothelial constitutive form of NOS (ecNOS) in vascular endothelium and inducible form of NOS (iNOS) in myometrial and vascular smooth muscle and in decidual epithelium. Immunoblotting revealed that expression of iNOS declined nearly fivefold, whereas ecNOS declined twofold in laboring rats at term. We conclude that iNOS is expressed in myometrium of pregnant rat uterus but not the virgin rat and that iNOS expression declines at term when labor is present. The pattern of changes in myometrial iNOS expression with advancing gestation suggests that NO could act in an autocrine and/or paracrine manner to inhibit uterine contractions before term.
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Tyson-Capper, A. J., E. A. Shiells, and S. C. Robson. "Interplay between polypyrimidine tract binding protein-associated splicing factor and human myometrial progesterone receptors." Journal of Molecular Endocrinology 43, no. 1 (April 1, 2009): 29–41. http://dx.doi.org/10.1677/jme-09-0001.
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The precise molecular mechanisms controlling progesterone receptor (PR)-mediated gene regulation within the human myometrium in pregnancy and in labour remain poorly defined. PR recruit different nuclear co-activators/co-repressors to mediate receptor-specific transcription regulation and expression of PR, and these co-factors may alter within the myometrium during pregnancy and labour. The aims of this study were to test the hypotheses that i) the human splicing and transcription factor, polypyrimidine tract binding protein-associated splicing factor (PSF), is spatially and temporally regulated in the myometrium during pregnancy and labour; ii) PSF influences the expression of myometrial PR and iii) the action of PR in regulating specific hormone response target genes in the human myometrium may involve PSF. Immunoblotting indicated that PSF expression is significantly up-regulated within the human myometrium as pregnancy progresses, in particular within the upper uterine region, and levels remain elevated in labour. Co-immunoprecipitations and DNA-binding assays show that PSF directly interacts with nuclear PR and glucocorticoid receptor (GR) and specific co-regulatory proteins, all of which have defined roles as co-activators or co-repressors in gene regulation. Over-expression and inhibition of PSF by transient transfection and RNAi respectively alters expression of myometrial PR and GR and may influence expression of two PR/GR-target genes, cyclooxygenase-2 and histone deacetylase-2. These findings are suggestive of a role for myometrial PSF as a nuclear co-regulator in the regulation of specific hormone receptor genes and their target hormone response genes.