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Artykuły w czasopismach na temat „Mice Fertility”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 28 stycznia 2023

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1

Boughton, Barbara. "Fertility preserved in irradiated mice." Lancet Oncology 3, no. 10 (October 2002): 584. http://dx.doi.org/10.1016/s1470-2045(02)00884-7.

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El-Fiky, B. A. "fertility in induced azoospermic mice." Journal of Bioscience and Applied Research 2, no. 9 (September 23, 2016): 626–33. http://dx.doi.org/10.21608/jbaar.2016.109004.

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Chubb, C., and L. Henry. "The fertility of hypothyroid male mice." Reproduction 83, no. 2 (July 1, 1988): 819–23. http://dx.doi.org/10.1530/jrf.0.0830819.

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Silberner, J. "Fertility Factor from the Mouths of Mice." Science News 130, no. 9 (August 30, 1986): 135. http://dx.doi.org/10.2307/3970946.

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Yamamoto, Yoshiko, Keiichi Yamamoto, and Tamaki Hayase. "Effect of Methamphetamine on Male Mice Fertility." Journal of Obstetrics and Gynaecology Research 25, no. 5 (October 1999): 353–58. http://dx.doi.org/10.1111/j.1447-0756.1999.tb01176.x.

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Rubinstein, Eric, Ahmed Ziyyat, Michel Prenant, Edyta Wrobel, Jean-Philippe Wolf, Shoshana Levy, François Le Naour, and Claude Boucheix. "Reduced fertility of female mice lacking CD81." Developmental Biology 290, no. 2 (February 2006): 351–58. http://dx.doi.org/10.1016/j.ydbio.2005.11.031.

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7

Gao, Qian, Li-Li Sun, Fen-Fen Xiang, Li Gao, Yin Jia, Jian-Rong Zhang, Hai-Bo Tao, Jun-Jie Zhang, and Wen-Jie Li. "Crybb2 deficiency impairs fertility in female mice." Biochemical and Biophysical Research Communications 453, no. 1 (October 2014): 37–42. http://dx.doi.org/10.1016/j.bbrc.2014.09.049.

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Evans, Maggie C., Mohammed Z. Rizwan, and Greg M. Anderson. "Insulin Action on GABA Neurons Is a Critical Regulator of Energy Balance But Not Fertility in Mice." Endocrinology 155, no. 11 (November 1, 2014): 4368–79. http://dx.doi.org/10.1210/en.2014-1412.

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Abstract Insulin signaling in the brain plays an important role in the central regulation of energy homeostasis and fertility, such that mice exhibiting brain-specific deletion of insulin receptors (InsRs) display a diet-sensitive obesogenic phenotype and hypothalamic hypogonadism. However, the specific neurons mediating insulin's central effects on fertility remain largely unidentified. The neurotransmitters γ-aminobutyric acid (GABA) and glutamate are important modulators of fertility and energy homeostasis and are widely distributed in the hypothalamus. We therefore investigated whether ins

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9

Kuchmiy, Anna A., Jinke D’Hont, Tino Hochepied, and Mohamed Lamkanfi. "NLRP2 controls age-associated maternal fertility." Journal of Experimental Medicine 213, no. 13 (November 23, 2016): 2851–60. http://dx.doi.org/10.1084/jem.20160900.

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Nucleotide-binding domain and leucine-rich repeat (NLR) proteins are well-known for their key roles in the immune system. Ectopically expressed NLRP2 in immortalized cell lines assembles an inflammasome and inhibits activation of the proinflammatory transcription factor NF-κB, but the physiological roles of NLRP2 are unknown. Here, we show that Nlrp2-deficient mice were born with expected Mendelian ratios and that Nlrp2 was dispensable for innate and adaptive immunity. The observation that Nlrp2 was exclusively expressed in oocytes led us to explore the role of Nlrp2 in parthenogenetic activat

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10

Hardy, C. M., J. F. M. ten Have, K. J. Mobbs, and L. A. Hinds. "Assessment of the immunocontraceptive effect of a zona pellucida 3 peptide antigen in wild mice." Reproduction, Fertility and Development 14, no. 3 (2002): 151. http://dx.doi.org/10.1071/rd01112.

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Immunizing laboratory mice against a short peptide to mouse zona pellucida protein 3 (mZP3; amino acids 328-342) reduces fertility in some strains. This antigen was therefore tested to see if it is suitable for use in an immunocontraceptive vaccine to control wild mice. Mouse zona pellucida protein 3 peptide conjugated to a carrier protein (keyhole limpet hemocyanin) was considerably more immunogenic and effective in reducing fertility in wild mice when compared with inbred BALB/c mice. Fertility of the immunized wild mice was reduced by over 50% compared with controls, whereas BALB/c mice sho

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11

Herbison, Allan E., Robert Porteous, Jean-Rémi Pape, Jocelyn M. Mora, and Peter R. Hurst. "Gonadotropin-Releasing Hormone Neuron Requirements for Puberty, Ovulation, and Fertility." Endocrinology 149, no. 2 (November 15, 2007): 597–604. http://dx.doi.org/10.1210/en.2007-1139.

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The absolute requirement for reproduction implies that the hypothalamo-pituitary-gonadal axis, controlling fertility, is an evolutionary robust mechanism. The GnRH neurons of the hypothalamus represent the key cell type within the body dictating fertility. However, the level of functional redundancy within the GnRH neuron population is unknown. As a result of a fortuitous transgene insertion event, GNR23 mice exhibit a marked allele-dependent reduction in GnRH neuron number within their brain. Wild-type mice have approximately 600 GnRH neurons, compared with approximately 200 (34%) and approxi

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12

Zhao, Longmei, Kerstin Reim, and David J. Miller. "Complexin-I-deficient sperm are subfertile due to a defect in zona pellucida penetration." REPRODUCTION 136, no. 3 (September 2008): 323–34. http://dx.doi.org/10.1530/rep-07-0569.

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Upon adhesion to the zona pellucida, sperm undergo regulated exocytosis of the acrosome. Although it is necessary for sperm to penetrate the zona pellucida and fertilize an egg, the acrosomal membrane fusion process is poorly understood. Complexins I and II are small, cytosolic proteins that bind to a complex of proteins termed the solubleN-ethylmaleimide-sensitive factor attachment protein receptor complex to regulate synaptic vesicle exocytosis. Complexin-II-deficient mice are fertile but the fertility of sperm from complexin-I-deficient male mice is unclear because the mice have ataxia and

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13

Yang, Jasmine J., Claudia S. Caligioni, Yee-Ming Chan, and Stephanie B. Seminara. "Uncovering Novel Reproductive Defects in Neurokinin B Receptor Null Mice: Closing the Gap Between Mice and Men." Endocrinology 153, no. 3 (March 1, 2012): 1498–508. http://dx.doi.org/10.1210/en.2011-1949.

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Patients bearing mutations in TAC3 and TACR3 (which encode neurokinin B and its receptor, respectively) have sexual infantilism and infertility due to GnRH deficiency. In contrast, Tacr3−/− mice have previously been reported to be fertile. Because of this apparent phenotypic discordance between mice and men bearing disabling mutations in Tacr3/TACR3, Tacr3 null mice were phenotyped with close attention to pubertal development, estrous cyclicity, and fertility. Tacr3−/− mice demonstrated normal timing of preputial separation and day of first estrus, markers of sexual maturation. However, at pos

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14

Maccarinelli, Federica, Maria Regoni, Fernando Carmona, Maura Poli, Esther G. Meyron-Holtz, and Paolo Arosio. "Mitochondrial ferritin deficiency reduces male fertility in mice." Reproduction, Fertility and Development 29, no. 10 (2017): 2005. http://dx.doi.org/10.1071/rd16348.

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Mitochondrial ferritin (FtMt) is a functional ferritin targeted to mitochondria that is highly expressed in the testis. To investigate the role of FtMt in the testis we set up a series of controlled matings between FtMt gene-deletion mice (FtMt–/–) with FtMt+/+ mice. We found that the number of newborns per litter and the fertility rate were strongly reduced for the FtMt–/– males, but not for the females, indicating that FtMt has an important role for male fertility. The morphology of the testis and of the spermatozoa of FtMt–/– mice was normal and we did not detect alterations in sperm parame

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15

Wood, H. M., U. J. Lee, D. Vurbic, E. Sabanegh, J. H. Ross, T. Li, and M. S. Damaser. "Sexual Development and Fertility of Loxl1-/- Male Mice." Journal of Andrology 30, no. 4 (February 5, 2009): 452–59. http://dx.doi.org/10.2164/jandrol.108.006122.

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Daigle,Jr., Harold J., Derek N. Cole, J. Andrew Carlson, William R. Lee, and Vincent L. Wilson. "Ethylene Dichloride Disruption of Fertility in Male Mice." Open Toxicology Journal 3, no. 1 (April 20, 2009): 39–46. http://dx.doi.org/10.2174/1874340400903010039.

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Hani, Toshio, Takanori Tachibe, Saburo Shingai, Nobuo Kamada, Otoya Ueda, and Kou-ichi Jishage. "Fertility of mice receiving vitrified adult mouse ovaries." Reproduction 131, no. 4 (April 2006): 681–87. http://dx.doi.org/10.1530/rep.1.01030.

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Cryopreservation of the ovaries is a useful technology for preservation of germ cells from experimental animals, because if the female founder is infertile or has mutated mitochondrial DNA, preservation of female germ cells is necessary. Although it is possible to cryopreserve immature mouse ovaries with a high degree of viability by vitrification with a mixture of several cryoprotectants, the viability of cryopreserved adult mouse ovaries is still unknown. Here, we investigated the viability of mouse ovaries at various ages after cryopreservation by vitrification techniques. Donor ovaries wer

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18

Umesaki, Naohiko, Satoshi Uda, Masami Kawabata, and Sachio Ogita. "Significance of peritoneal macrophages on fertility in mice." American Journal of Obstetrics and Gynecology 167, no. 1 (July 1992): 261–64. http://dx.doi.org/10.1016/s0002-9378(11)91671-8.

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deCatanzaro, Denys. "Duration of mating relates to fertility in mice." Physiology & Behavior 50, no. 2 (August 1991): 393–95. http://dx.doi.org/10.1016/0031-9384(91)90084-2.

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Le Naour, F. "Severely Reduced Female Fertility in CD9-Deficient Mice." Science 287, no. 5451 (January 14, 2000): 319–21. http://dx.doi.org/10.1126/science.287.5451.319.

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Kanatsu-Shinohara, M., H. Miki, K. Inoue, N. Ogonuki, S. Toyokuni, A. Ogura, and T. Shinohara. "Germline niche transplantation restores fertility in infertile mice." Human Reproduction 20, no. 9 (May 26, 2005): 2376–82. http://dx.doi.org/10.1093/humrep/dei096.

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Fan, Shutong, Yuhan Zhao, Zhiwei Pan, Zhiqin Gao, Zumu Liang, Zhifang Pan, and Weiguo Feng. "ZNF185-derived peptide induces fertility suppression in mice." Journal of Peptide Science 24, no. 10 (September 17, 2018): e3121. http://dx.doi.org/10.1002/psc.3121.

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Su, Weiheng, Ying Qiao, Fei Yi, Xingang Guan, Di Zhang, Shuzhi Zhang, Feng Hao, et al. "Increased female fertility in aquaporin 8-deficient mice." IUBMB Life 62, no. 11 (November 2010): 852–57. http://dx.doi.org/10.1002/iub.398.

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Schoeller, Erica L., Maggie Chi, Andrea Drury, Ashley Bertschinger, Prabagaran Esakky, and Kelle H. Moley. "Leptin Monotherapy Rescues Spermatogenesis in Male Akita Type 1 Diabetic Mice." Endocrinology 155, no. 8 (August 1, 2014): 2781–86. http://dx.doi.org/10.1210/en.2014-1119.

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Type 1 diabetes is associated with subfertility in humans. The current treatment for type 1 diabetes, insulin monotherapy, is suboptimal to fully stabilize glycemia, potentially leading to this subfertility. Recent work has demonstrated that treatment with the energy-regulating hormone leptin, alone or in combination with insulin, can more effectively control glycemia in mouse models of type 1 diabetes. Here, we sought to determine whether the fertility defects in a type 1 diabetic mouse model, the Akita mouse, can be rescued with leptin monotherapy in the absence of any exogenous insulin. Aki

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Singireddy, Amritha V., Megan A. Inglis, Wieteke A. Zuure, Joon S. Kim, and Greg M. Anderson. "Neither Signal Transducer and Activator of Transcription 3 (STAT3) or STAT5 Signaling Pathways Are Required for Leptin's Effects on Fertility in Mice." Endocrinology 154, no. 7 (May 21, 2013): 2434–45. http://dx.doi.org/10.1210/en.2013-1109.

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Abstract The hormone leptin is critical for the regulation of energy balance and fertility. The long-form leptin receptor (LepR) regulates multiple intracellular signaling cascades, including the classic Janus kinase-signal transducer and activator of transcription (STAT) pathways. Previous studies have shown that deletion of STAT3 or the closely related STAT5 from the brain results in an obese phenotype, but their roles in fertility regulation are not clear. This study tested whether STAT3 and STAT5 pathways of leptin signaling are required for fertility, and whether absence of one pathway mi

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Chen, Yinghong, Chao Liu, Yongliang Shang, Liying Wang, Wei Li, and Guoping Li. "Adam21 is dispensable for reproductive processes in mice." PeerJ 9 (September 23, 2021): e12210. http://dx.doi.org/10.7717/peerj.12210.

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Background As a group of membrane-anchored proteins, the proteins containing a disintegrin and metalloprotease domain (ADAMs) control many biological processes, especially for male fertility. Mouse Adam21 was previously found to be specifically expressed in the somatic cells and germ cells of testes, but its functional role during spermatogenesis and male reproductive processes is still unknown. Methods Adam21-null mice were created using the CRISPR/Cas9 system. Quantitative real-time PCR was used for analyzing of gene expression. Histological, cytological and immunofluorescence staining were

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Burton, Kimberly A., and G. Stanley McKnight. "PKA, Germ Cells, and Fertility." Physiology 22, no. 1 (February 2007): 40–46. http://dx.doi.org/10.1152/physiol.00034.2006.

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Temporal and spatial regulation of PKA activity are essential for vigorous sperm motility and for the resumption of meiosis in oocytes, two events required for successful fertilization. Genetic mutations in mice that affect PKA signaling in germ cells lead to infertility and illustrate the importance of this pathway in mammalian reproduction.

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Jacob, Jens, Grant R. Singleton, and Lyn A. Hinds. "Fertility control of rodent pests." Wildlife Research 35, no. 6 (2008): 487. http://dx.doi.org/10.1071/wr07129.

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Ricefield rats (Rattus argentiventer) in south-east Asian rice fields and house mice (Mus domesticus) in Australian grain fields are major pest species. They cause damage before and after harvest and carry zoonotic diseases. For both species, management techniques have been pursued using the approach of immunocontraceptive vaccination. We review results from a series of enclosure and field studies conducted with these species to assess the effects of fertility control in small rodents. In the experiments, fertility control was simulated by tubal ligation, ovariectomy or progesterone treatment.

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Xiao, Yuhang, Baojun Xu, Matteo Bordiga, Haiwei Li, Fabiano Travaglia, Shun Bai, Jiali Chen, and Weibin Bai. "Cyanidin-3-O-Glucoside Supplement Improves Sperm Quality and Spermatogenesis in a Mice Model of Ulcerative Colitis." Nutrients 14, no. 5 (February 25, 2022): 984. http://dx.doi.org/10.3390/nu14050984.

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Impaired fertility and low sperm quality are the global health problem with high attention. It has been noted that inflammation may impact fertility by affecting testicular spermatogenesis. Cyanidin-3-O-glucoside is a natural functional pigment with various health benefits. Nevertheless, studies on the mechanism by which C3G protects male reproduction in mice with ulcerative colitis remain scarce. The purpose of this study is to illustrate the potential mechanism of C3G for improving impaired fertility caused by colitis. A DSS-induced colitis model was applied to assess the effects of sperm qu

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Abbasi, Ferheen, Mayo Kodani, Chihiro Emori, Daiji Kiyozumi, Masashi Mori, Yoshitaka Fujihara, and Masahito Ikawa. "CRISPR/Cas9-Mediated Genome Editing Reveals Oosp Family Genes are Dispensable for Female Fertility in Mice." Cells 9, no. 4 (March 28, 2020): 821. http://dx.doi.org/10.3390/cells9040821.

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There are over 200 genes that are predicted to be solely expressed in the oocyte and ovary, and thousands more that have expression patterns in the female reproductive tract. Unfortunately, many of their physiological functions, such as their roles in oogenesis or fertilization, have yet to be elucidated. Previous knockout (KO) mice studies have proven that many of the genes that were once thought to be essential for fertility are dispensable in vivo. Therefore, it is extremely important to confirm the roles of all genes before spending immense time studying them in vitro. To do this, our labo

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Guo, Tao, Liang Zhang, Dong Cheng, Tao Liu, Liguo An, Wei-Ping Li, and Cong Zhang. "Low-density lipoprotein receptor affects the fertility of female mice." Reproduction, Fertility and Development 27, no. 8 (2015): 1222. http://dx.doi.org/10.1071/rd13436.

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Low-density lipoprotein receptor (LDLR) has been demonstrated to play a central role in lipoprotein metabolism, with Ldlr-deficient (Ldlr–/–) mice developing severe dyslipidemia. In the present study we investigated whether Ldlr knockout could harm female reproduction and explored the mechanisms involved. The results indicate that although the number of litters born to Ldlr–/– mice did not differ significantly from that born to controls, the number of pups per litter was significantly lower in the former group. Interestingly, although Ldlr–/– mice were obese, the weight of their ovaries was lo

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Rodrigo, Natassia, Hui Chen, Carol A. Pollock, and Sarah J. Glastras. "Preconception weight loss improves fertility and maternal outcomes in obese mice." Journal of Endocrinology 253, no. 1 (April 1, 2022): 27–38. http://dx.doi.org/10.1530/joe-21-0399.

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Women with obesity have higher incidences of infertility, with longer time to conception and increased risk of pregnancy complications compared to women with normal body weight. There is a lack of evidence demonstrating the benefit of preconception maternal weight loss on fertility and pregnancy outcomes. We aimed to determine if preconception weight loss, either with diet modification or glucose-like peptide 1 receptor agonist liraglutide, improves maternal weight, fertility, and pregnancy outcomes. C57BL/6 female mice were fed either a high-fat diet (HFD) or chow for 8 weeks. HFD-fed dams we

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Navarro-Pando, José M., Elísabet Alcocer-Gómez, Beatriz Castejón-Vega, Elena Navarro-Villarán, Mónica Condés-Hervás, María Mundi-Roldan, Jordi Muntané, et al. "Inhibition of the NLRP3 inflammasome prevents ovarian aging." Science Advances 7, no. 1 (January 2021): eabc7409. http://dx.doi.org/10.1126/sciadv.abc7409.

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Inflammation is a hallmark of aging and is negatively affecting female fertility. In this study, we evaluate the role of the NLRP3 inflammasome in ovarian aging and female fertility. Age-dependent increased expression of NLRP3 in the ovary was observed in WT mice during reproductive aging. High expression of NLRP3, caspase-1, and IL-1β was also observed in granulosa cells from patients with ovarian insufficiency. Ablation of NLRP3 improved the survival and pregnancy rates and increased anti-Müllerian hormone levels and autophagy rates in ovaries. Deficiency of NLRP3 also reduced serum FSH and

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Sitasiwi, Agung Janika, Sri Isdadiyanto, and Siti Muflichatun Mardiati. "Pelacakan eskpresi protein pada testis mencit (Mus musculus) setelah paparan esktrak etanol daun mimba (Azadirachta indica)." Jurnal Sain Veteriner 37, no. 1 (August 5, 2019): 90. http://dx.doi.org/10.22146/jsv.43027.

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Abstract Azadirachta indica (Neem) has been shown to affect the fertility of mice by interfering with the synthesis of testosterone in mice. The aim of this study was to detect the testes protein expression of mice after exposure to the ethanolic Neem leaf extract. The laboratory animals of this study were 20 male Swiss Webster mice with three months in age and body weight ranging from 27.5 grams. The mice were divided into two treatment groups, namely K (control group, exposed with distilled water) and P (treatment group, exposed to etahnolic Neem leaf extract with 14 mg/animal /day). The tre

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Wang, Yi-Bo, Chen-Yang Zhai, Guan-Ping Yao, Ting-Bao Chen, Lu-Lu Xue, Lin Zhou, Liu-Lin Xiong, and Ting-Hua Wang. "ATP5D Is a Potential Biomarker for Male Fertility." Oxidative Medicine and Cellular Longevity 2023 (January 11, 2023): 1–13. http://dx.doi.org/10.1155/2023/4923614.

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Background. Infertility is a global medical and social problem that affects human health and social development. At present, about 15% of couples of the right age in the world are infertile. As all we know, genetic defects are the most likely underlying cause of the pathology. ATP5D is also known as the delta subunit of mitochondrial ATP synthase. Mitochondria maintain sperm vitality, capacitation, acrosome reaction, and DNA integrity through ATP. Mitochondrial damage can trigger energy synthesis disorders, resulting in decreased sperm quality and function or even disappearance. The specific r

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Kobayashi, Kiyonori, Tsutomu Endo, Takafumi Matsumura, Yonggang Lu, Zhifeng Yu, Martin M. Matzuk, and Masahito Ikawa. "Prss55 but not Prss51 is required for male fertility in mice†." Biology of Reproduction 103, no. 2 (April 17, 2020): 223–34. http://dx.doi.org/10.1093/biolre/ioaa041.

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Abstract Mammalian spermatozoa are produced in the testis through spermatogenesis and matured in the epididymis to acquire fertilizing ability. Spermatozoa are ejaculated and migrate from the uterus to the oviducts to fuse with oocytes. Although over 2000 genes are expressed abundantly in mouse testes, the genes responsible for male fertility are not yet fully clarified. Here, we focused on two testis-enriched serine protease genes, Serine protease (Prss) 51 and Prss55, which overlap their gene loci partially in both mice and humans. To characterize their functions in male fertility, we first

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Kanellopoulos, Dimitrios, Dimitra Karagianni, Vasilios Pergialiotis, Nikolaos Nikiteas, Andreas C. Lazaris, and Dimitrios Iliopoulos. "The effect of endometriosis on fertility in an animal model." Journal of Medicine and Life 15, no. 9 (September 2022): 1170–75. http://dx.doi.org/10.25122/jml-2021-0391.

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The present experimental model aimed to investigate the possible effect of endometriosis on ovarian function by altering follicular maturation and development. This single-blind, randomized study included twenty-four female Sprague Dawley mice, 2.5 months old, weighing 160–200 grams. The animals were randomly separated into four groups on the day of the surgery. Each group consisted of 6 mice. The first group (A) consisted of healthy female mice (control group). The second group (B) consisted of mice subjected to surgical insertion of ovarian endometrioma. The third group (C) consisted of mice

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Krajnc-Franken, Magda A. M., Ad J. M. van Disseldorp, Jasper E. Koenders, Sietse Mosselman, Marcel van Duin, and Jan A. Gossen. "Impaired Nipple Development and Parturition in LGR7 Knockout Mice." Molecular and Cellular Biology 24, no. 2 (January 15, 2004): 687–96. http://dx.doi.org/10.1128/mcb.24.2.687-696.2004.

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ABSTRACT LGR7 is a G-protein coupled receptor with structural homology to the gonadotrophin and thyrotrophin receptors. Recently, LGR7 was deorphanized, and it was shown that relaxin is the ligand for LGR7. To further study the function of this receptor, mice deficient for LGR7 were generated by replacing part of the transmembrane-encoding region with a LacZ reporter cassette. Here we show that LGR7 is expressed in various tissues, including the uterus, heart, brain, and testis. Fertility studies using female LGR7−/− mice showed normal fertility and litter size. However, some females were inca

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Al-Hamood, M. H., A. Elbetieha, and H. Bataineh. "Sexual maturation and fertility of male and female mice exposed prenatally and postnatally to trivalent and hexavalent chromium compounds." Reproduction, Fertility and Development 10, no. 2 (1998): 179. http://dx.doi.org/10.1071/r97001.

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The reproductive toxicity of trivalent and hexavalent chromium compounds was investigated in male and female mice exposed to 1000 ppm chromium chloride and potassium dichromate via their mother during gestational and lactational periods. Fertility was reduced in male offspring exposed to either trivalent or hexavalent chromium compounds. Body weights and weights of testes, seminal vesicles and preputial glands were reduced in trivalent-exposed male offspring. The exposure of female mice offspring to trivalent and hexavalent chromium compounds delayed sexual maturation. Fertility was reduced in

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Wang, Tao, Binbin Cao, Yao Cai, Si Chen, Baozhu Wang, Yan Yuan, and Quan Zhang. "Plcz1 Deficiency Decreased Fertility in Male Mice Which Is Associated with Sperm Quality Decline and Abnormal Cytoskeleton in Epididymis." International Journal of Molecular Sciences 24, no. 1 (December 24, 2022): 314. http://dx.doi.org/10.3390/ijms24010314.

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Phospholipase C zeta1 (Plcz1) was known to be a physiological factor in sperm that activates oocytes to complete meiosis by triggering Ca2+ oscillations after fertilisation. However, the role of male Plcz1 in spermatogenesis and early embryo development in progeny has been controversial. Plcz1 knockout (Plcz1−/−) mouse model (Plcz1m3 and Plcz1m5) was generated by using the CRISPR-Cas9 system. The fertility of Plcz1−/− mice was evaluated by analysing the number of offsprings, sperm quality, pathological changes in the testis and epididymis. RNA-seq and RT-PCR were performed to screen differenti

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Tsutsumi, O., Y. Taketani, and T. Oka. "The uterine growth-promoting action of epidermal growth factor and its function in the fertility of mice." Journal of Endocrinology 138, no. 3 (September 1993): 437—NP. http://dx.doi.org/10.1677/joe.0.1380437.

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ABSTRACT Epidermal growth factor (EGF) levels in the submandibular glands and plasma are increased in pregnant and aged female mice. The possible role of EGF in fertility was studied in virgin and pregnant mice ranging in age from 10 to 90 weeks of age, employing sialoadenectomy, administration of EGF antibody and EGF replacement. The uterine weight in pregnant, 10-week-old, sialoadenectomized mice was significantly less than in normal mice and the administration of EGF antibody to these mice further decreased uterine weight, resulting in an increased rate of abortion. Replacement EGF treatmen

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Sato, Ban, Seiya Kanai, Daiki Sakaguchi, Kodai Yajima, Yu Matsumoto, Kazunori Morohoshi, Shinji Kagaya, et al. "Suppressive Role of Lactoferrin in Overweight-Related Female Fertility Problems." Nutrients 14, no. 5 (February 22, 2022): 938. http://dx.doi.org/10.3390/nu14050938.

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The secretory glycoprotein lactoferrin (LF) is suggested to ameliorate overweight regardless of non-genetic or genetic mechanisms. Although maternal overweight represents a key predictor of offspring growth, the efficacy of LF on fertility problems in overweight and obese mothers remains unknown. To address this issue, we examined the effect of LF ingestion by analyzing overweight mice (Institute of Cancer Research (ICR) mice with high-fat diets; HF mice) and obese mice (leptin-deficient mice with type II diabetes; ob/ob mice). Plasma insulin, leptin, glucose, and cholesterol levels were measu

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Powers, Natalie R., Beth L. Dumont, Chihiro Emori, Raman Akinyanju Lawal, Catherine Brunton, Kenneth Paigen, Mary Ann Handel, Ewelina Bolcun-Filas, Petko M. Petkov, and Tanmoy Bhattacharyya. "Sexual dimorphism in the meiotic requirement for PRDM9: A mammalian evolutionary safeguard." Science Advances 6, no. 43 (October 2020): eabb6606. http://dx.doi.org/10.1126/sciadv.abb6606.

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In many mammals, genomic sites for recombination are determined by the histone methyltransferase PRMD9. Some mouse strains lacking PRDM9 are infertile, but instances of fertility or semifertility in the absence of PRDM9 have been reported in mice, canines, and a human female. Such findings raise the question of how the loss of PRDM9 is circumvented to maintain fertility. We show that genetic background and sex-specific modifiers can obviate the requirement for PRDM9 in mice. Specifically, the meiotic DNA damage checkpoint protein CHK2 acts as a modifier allowing female-specific fertility in th

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Feng, Tianhao, Shushu Zhou, Xiaodan Shi, Xin Zhang, Jintao Zhang, Shuqin Zhao, Xiaoyu Yang, Xuhui Meng, and Mingxi Liu. "Eef2k is not required for fertility in male mice." Translational Andrology and Urology 10, no. 5 (May 2021): 1988–99. http://dx.doi.org/10.21037/tau-21-18.

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Wang, ZhiXin, Zi Teng, ZeLin Wang, Zhan Song, Peng Zhu, Ning Li, YuSheng Zhang, XueXia Liu, and FuJun Liu. "Melatonin ameliorates paclitaxel‐induced mice spermatogenesis and fertility defects." Journal of Cellular and Molecular Medicine 26, no. 4 (January 9, 2022): 1219–28. http://dx.doi.org/10.1111/jcmm.17177.

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Zudova, Dagmar, Andrew J. Wyrobek, Jack Bishop, and Francesco Marchetti. "Impaired fertility in T-stock female mice after superovulation." Reproduction 128, no. 5 (November 2004): 573–81. http://dx.doi.org/10.1530/rep.1.00333.

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Superovulation of female mice with exogenous gonadotrophins is routinely used for increasing the number of eggs ovulated by each female in reproductive and developmental studies. We report an unusual effect of superovulation on fertilization in mice.In vivomatings of superovulated T-stock females with B6C3F1 males resulted in a two-fold reduction (P< 0.001) in the frequencies of fertilized eggs compared with control B6C3F1 matings. In addition, approximately 22 h after mating, only 15% of fertilized eggs recovered in T-stock females had reached the metaphase stage of the first cleavage divi

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Thomas, A. "Growth hormone and fertility in oMt1a-oGH transgenic mice." Reproduction 122, no. 4 (October 1, 2001): 537–44. http://dx.doi.org/10.1530/reprod/122.4.537.

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Song, Ning, Fei Sun, Yu-Bing Dai, and Yu Lin. "LncRNA4667 is dispensable for spermatogenesis and fertility in mice." Reproductive and Developmental Medicine 3, no. 1 (2019): 18. http://dx.doi.org/10.4103/2096-2924.255985.

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Suzuki, Taichi A., and Michael W. Nachman. "Speciation and reduced hybrid female fertility in house mice." Evolution 69, no. 9 (September 2015): 2468–81. http://dx.doi.org/10.1111/evo.12747.

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Sainsbury, A. "Y4 receptor knockout rescues fertility in ob/ob mice." Genes & Development 16, no. 9 (May 1, 2002): 1077–88. http://dx.doi.org/10.1101/gad.979102.

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