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Lee, Dennis K., Victor R. Saldivia, Tuan Nguyen, Regina Cheng, Susan R. George, and Brian F. O’Dowd. "Modification of the Terminal Residue of Apelin-13 Antagonizes Its Hypotensive Action." Endocrinology 146, no. 1 (2005): 231–36. http://dx.doi.org/10.1210/en.2004-0359.
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The apelin peptide is the endogenous ligand for the apelin G protein-coupled receptor. The distribution of the apelin peptides and receptor are widespread in the central nervous system and periphery, with reported roles in the hypothalamic-pituitary-adrenal axis, blood pressure regulation and as one of the most potent positive inotropic substances yet identified. In this report, we show that in native tissues preproapelin exists as a dimer. Dimeric preproapelin was reduced to monomers by dithiothreitol treatment, indicating disulfide linkages. To evaluate the role of the carboxyl-terminal phenylalanine in the hypotensive action of apelin-13, analogs were generated and tested for their role on blood pressure regulation. Injections of apelin-13 and apelin-12 (15 μg/kg) into spontaneously hypertensive rats lowered systolic and diastolic blood pressure to result in decreases of approximately 60% and 15% in mean arterial blood pressure, respectively. Apelin-13(13[d-Phe]) treatment did not differ from apelin-13 in either efficacy or duration of effect, whereas apelin-13(F13A) revealed a loss of function. However, concomitant administration of apelin-13(F13A) (30 μg/kg) blocked hypotensive effects of apelin-13 (15 μg/kg), which revealed that apelin-13(F13A) behaved as an apelin-specific antagonist.
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Fernandez, Kleinberg X., Conrad Fischer, Jennie Vu, et al. "Metabolically stable apelin-analogues, incorporating cyclohexylalanine and homoarginine, as potent apelin receptor activators." RSC Medicinal Chemistry 12, no. 8 (2021): 1402–13. http://dx.doi.org/10.1039/d1md00120e.
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Besserer-Offroy, Élie, Patrick Bérubé, Jérôme Côté та ін. "The hypotensive effect of activated apelin receptor is correlated with β-arrestin recruitment". Pharmacological Research 131 (травень 2018): 7–16. http://dx.doi.org/10.1016/j.phrs.2018.02.032.
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Zhang, Rong, Jingyi Lu, Cheng Hu, et al. "Associations of Common Variants atAPLNand Hypertension in Chinese Subjects with and without Diabetes." Experimental Diabetes Research 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/917496.
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Background. Apelin, the endogenous ligand for the APJ receptor, has a potent hypotensive effect via a nitric oxide-dependent mechanism in vivo. The aim of the study was to investigate the association between the common variants of apelin gene (APLN) and hypertension, which was reported recently in a Chinese Han population with and without diabetes.Methods. Three single nucleotide polymorphisms (SNPs) onAPLNwere genotyped in 3156 diabetic patients and 3736 nondiabetic individuals. For non-diabetic subjects, 1779 were enrolled in stage 1 and 1757 were recruited for validation. A meta-analysis combining the two stages was carried out to obtain the overall effect.Results. In diabetic patients, no significant associations of the three SNPs with hypertension were observed. In contrast, we found that rs2235306 was associated with hypertension in non-diabetic males after adjusting for covariates (OR=1.19,P=0.039) while rs2235307 and rs3115759 displayed no evidence of association in both genders. One haplotype, C-C-A, also showed an association with hypertension (OR=1.47,P=0.032) only in men. However, analysis in stage 2 and meta-analysis did not support these findings.Conclusions. We conclude that common variants onAPLNare not associated with the prevalence of hypertension in the Chinese.
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Trojanowicz, Bogusz, Christof Ulrich, and Matthias Girndt. "Uremic Apelin and Leucocytic Angiotensin-Converting Enzyme 2 in CKD Patients." Toxins 12, no. 12 (2020): 742. http://dx.doi.org/10.3390/toxins12120742.
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Apelin peptides (APLN) serve as second substrates for angiotensin-converting enzyme 2 (ACE2) and, in contrast to angiotensin II (AngII), exert blood-pressure lowering and vasodilatation effects through binding to G-coupled APLN receptor (APLNR). ACE2-mediated cleavage of the APLN may reduce its vasodilatory effects, but decreased ACE2 may potentiate the hypotensive properties of APLN. The role of APLN in uremia is unclear. We investigated the correlations between serum-APLN, leucocytic APLNR, and ACE2 in 32 healthy controls (NP), 66 HD, and 24 CKD3–5 patients, and the impact of APLN peptides on monocytic behavior and ACE2 expression under uremic conditions in vitro. We observed that serum APLN and leucocytic APLNR or SLCO2B1 were significantly elevated in uremic patients and correlated with decreased ACE2 on uremic leucocytes. APLN-treated THP-1 monocytes revealed significantly increased APLNR and ACE2, and reduced TNFa, IL-6, and MCSF. Uremic toxins induced a dramatic increase of miR-421 followed by significant reduction of ACE2 transcripts, partially counteracted with APLN-13 and -36. APLN-36 triggered the most potent transmigration and reduction of endothelial adhesion. These results suggest that although APLN peptides may partly protect against the decay of monocytic ACE2 transcripts, uremic milieu is the most dominant modulator of local ACE2, and likely to contribute to the progression of atherosclerosis.
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Пальцын, А. А., and Н. Б. Свиридкина. "Apelin." Nauchno-prakticheskii zhurnal «Patogenez», no. 2 (June 28, 2021): 83–90. http://dx.doi.org/10.25557/2310-0435.2021.02.83-90.
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Апелин - слово, появившееся в 1998 году. Так, по аббревиатуре рецептора APJ, авторы назвали, найденный ими лиганд этого рецептора. Существует в нескольких изоформах, от 13 до 77 аминокислотных остатков. Наиболее активна самая короткая форма: апелин-13. Образуется жировой и мышечной тканью - адипокин и миокин. В экспериментах на мышах обнаружено много положительных эффектов действия апелина, в том числе торможение развития старости. В нарастающем потоке клинических результатов есть сообщения о благоприятном действии апелина при нарушениях энергетического обмена, сердечно-сосудистой патологии, гипоксических состояниях, саркопении, ожирении, диабете. Apelin is a word that emerged in 1998. This is how the authors named the APJ receptor ligand they discovered, by the abbreviation of this receptor. Apelin exists in several isoforms ranging in size from 13 to 77 amino acid residues. The shortest form, apelin-13, is the most active one. Apelin is produced by adipose and muscle tissue as an adipokine and a myokine. Experiments on mice have shown multiple beneficial effects of apelin, including slowing the ageing process. In the growing stream of clinical results, there are reports of the beneficial effect of apelin in disorders of energy metabolism, cardiovascular diseases, hypoxic conditions, sarcopenia, obesity, and diabetes mellitus.
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SUZUKI, KEIKO. "Studies on estimation of hypotensive effect by hypotensive drugs." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 21, no. 1 (1990): 143–44. http://dx.doi.org/10.3999/jscpt.21.143.
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Abdul-Ghani, A. S., R. Amin, and M. S. Suleiman. "Hypotensive Effect ofCrataegus oxyacantha." International Journal of Crude Drug Research 25, no. 4 (1987): 216–20. http://dx.doi.org/10.3109/13880208709055196.
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Villar, A., M. J. Sanz, and M. Paya. "Hypotensive Effect ofPistacia lentiscusL." International Journal of Crude Drug Research 25, no. 1 (1987): 1–3. http://dx.doi.org/10.3109/13880208709060902.
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PRIETO, Juan Carlos, Mónica QUEVEDO, Hugo F. MIRANDA, and Gianni PINARDI. "Hypotensive effect of dopamine." Acta Cardiologica 60, no. 3 (2005): 253–57. http://dx.doi.org/10.2143/ac.60.3.2005004.
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Henley, David E., Fiona Buchanan, Rosemary Gibson, et al. "Plasma apelin levels in obstructive sleep apnea and the effect of continuous positive airway pressure therapy." Journal of Endocrinology 203, no. 1 (2009): 181–88. http://dx.doi.org/10.1677/joe-09-0245.
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Apelin is a peptide hormone with cardiovascular and glucose homeostasis properties, and obstructive sleep apnea (OSA) is complicated by cardiovascular and metabolic comorbidities. Plasma apelin has not been previously assessed in OSA. We investigated the response of plasma apelin to a 2-h 75 g oral glucose tolerance test (OGTT) and the effect of 3 months compliant continuous positive airway pressure (CPAP) therapy in 15 obese males with newly diagnosed OSA. Plasma apelin and serum cortisol were recorded 10 minutely, while serum insulin and glucose were measured 30 minutely. Ten subjects had plasma apelin measured at intervals across a 24-h period to investigate for circadian variation in apelin levels, and this was repeated following 3 months compliant CPAP therapy. Fasting (0.342±0.038 vs 0.288±0.024 ng/ml, P=0.04), 30 min (0.399±0.035 vs 0.312±0.036 ng/ml, P=0.007) and 120 min (0.402±0.030 vs 0.259±0.024 ng/ml, P<0.001) apelin levels were reduced following CPAP. The area under curve for apelin OGTT response was lower post-CPAP (44.1±3.3 vs 35.8±2.3 ng/ml per min, P<0.001). Mean OGTT apelin levels showed a significant treatment effect (P=0.006) and a time effect (P<0.001), and the effect of time was different pre- versus post-CPAP (P=0.005). No significant variability in apelin levels existed across the 24-h period at diagnosis. Lower levels were evident overnight following treatment (P=0.004). Improvements in insulin and glucose parameters and reduced cortisol levels were found post-CPAP. In summary, untreated OSA was associated with elevated plasma apelin levels, altered apelin secretory dynamics in response to oral glucose and lack of an apparent circadian variability, which was restored following CPAP.
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Birsen, İlknur, V. Nimet İzgüt-Uysal, Hakan Soylu, and İsmail Üstünel. "The effect of apelin-13 on gastric ischemia/reperfusion injury: the roles of sensory nerves and vagus nerve." Canadian Journal of Physiology and Pharmacology 98, no. 5 (2020): 282–95. http://dx.doi.org/10.1139/cjpp-2019-0502.
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Apelin is a peptide that plays a role in physiological processes such as angiogenesis, apoptosis, and proliferation. The aim of this study was to investigate the role of capsaicin-sensitive afferent neurons and vagus in the effect of apelin against ischemia/reperfusion (I/R) injury. The experimental groups were (1) control, (2) I/R, (3) apelin + I/R, (4) vagotomy + I/R, (5) vagotomy + apelin + I/R, (6) capsaicin + I/R, (7) capsaicin + apelin + I/R, (8) lorglumide + I/R, and (9) lorglumide + apelin + I/R. To test the potential gastroprotective effect of apelin-13, apelin-13 (2 mg/kg i.v.) was administered just before both ischemia and reperfusion. A vagotomy was performed 1 week before I/R in the vagotomized groups; capsaicin (125 mg/kg s.c.) was administrated 2 weeks before I/R in the capsaicin-treated groups and lorglumide (5 mg/kg i.p.) was administered 30 min before I/R in the lorglumide-treated groups. After I/R, a variety parameters in gastric tissue were analyzed. cfos expression was determined in brainstem samples. In the I/R group, the lesion index, myeloperoxidase activity, lipid peroxidation, nitric oxide, and tumor necrosis factor-α increased, and mucosal blood flow, prostaglandin-E2, and calcitonin gene related peptide decreased. Apelin prevented the damaging effects of I/R and increased cfos expression in brainstem areas. Vagotomy, capsaicin, and lorglumide largely eliminated the gastroprotective effects of apelin-13. This study showed that sensory nerves and the vagus play regulatory roles in apelin-induced gastroprotection. Cholecystokinin may play a role in the effect of apelin through sensory neurons.
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Benk Silfeler, Dilek, Cumali Gokce, Raziye Keskin Kurt, et al. "Does Polycystic Ovary Syndrome Itself Have Additional Effect on Apelin Levels?" Obstetrics and Gynecology International 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/536896.
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Objective. The present study was designed to compare serum levels of apelin between lean PCOS women and healthy women with regular menses.Study Design. A total of 30 lean patients with PCOS and 30 healthy subjects were included in this study. Serum apelin levels were compared between groups.Results. Serum apelin levels in lean PCOS patients were not significantly different from the control subjects.Conclusion. Our findings indicate that PCOS itself does not seem to change apelin levels. Further investigation on a large number of subjects will need to be conducted to prove the consistent or variable association in PCOS.
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Murza, Alexandre, Élie Besserer-Offroy, Jérôme Côté, et al. "C-Terminal Modifications of Apelin-13 Significantly Change Ligand Binding, Receptor Signaling, and Hypotensive Action." Journal of Medicinal Chemistry 58, no. 5 (2015): 2431–40. http://dx.doi.org/10.1021/jm501916k.
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Castan-Laurell, Isabelle, Michaela Vítkova, Danièle Daviaud, et al. "Effect of hypocaloric diet-induced weight loss in obese women on plasma apelin and adipose tissue expression of apelin and APJ." European Journal of Endocrinology 158, no. 6 (2008): 905–10. http://dx.doi.org/10.1530/eje-08-0039.
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ObjectiveApelin is a novel adipokine acting on APJ receptor, regulated by insulin and tumor necrosis factor-α (TNF-α) in adipose tissue (AT). Plasma apelin levels are increased in obese hyperinsulinemic subjects. The aim was to investigate whether the hypocaloric diet associated with weight loss modifies the elevated plasma apelin levels and the expression of apelin and APJ receptor in AT in obese women.Design and methodsFasting plasma levels of apelin and TNF-α as well as mRNA levels of apelin and APJ in AT were measured before and after a 12-week hypocaloric weight-reducing diet in 20 obese women (body mass index (BMI) before diet 32.2±6.4 kg/m2). Twelve healthy women with a BMI of 20.7±0.6 kg/m2 served as reference.ResultsPlasma levels of apelin and TNF-α were higher in obese compared with lean controls. The hypocaloric diet resulted in a significant decrease of BMI to 29.8±6.3 kg/m2, plasma insulin (8.16±0.73 to 6.58±0.66 mU/l), apelin (369±25 pg/ml to 257±12 pg/ml), TNF-α levels (0.66±0.04 pg/ml to 0.56±0.04 pg/ml), and AT mRNAs of apelin and APJ. In addition, changes in AT mRNA apelin were related to changes in AT mRNA APJ levels.ConclusionThe hypocaloric diet associated with weight loss reduces the increased plasma and AT expression of apelin in obese women. This reduced apelin expression in AT could contribute to decreased circulating apelin levels.
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Kutlay, Özden, Arzu Keskin Aktan, and Esra Aslan. "The protective effect of apelin-13 on cardiorenal toxicity induced by cyclophosphamide." Canadian Journal of Physiology and Pharmacology 100, no. 4 (2022): 314–23. http://dx.doi.org/10.1139/cjpp-2021-0337.
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Cyclophosphamide is a chemotherapeutic drug that is widely used in the clinic and can cause multi-organ toxicity. Apelin-13 is an endogenous adipocytokine with antioxidant properties. Therefore, this study investigated the possibility of apelin-13 being a potential therapeutic agent on cardiac toxicity and nephrotoxicity caused by cyclophosphamide. In this study, a total of four groups were formed with eight rats in each group. Group I: the control group was administered only saline (i.p.). Group II: cyclophosphamide, a single dose of 200 mg/kg (i.p.) on day 7. Group III: apelin-13 (15 μg/kg), for 7 days (i.p.). Group IV: administered apelin-13 (15 μg/kg) (i.p.) for 7 days and a single dose of cyclophosphamide (200 mg/kg) (i.p.) on day 7, the rats were sacrificed on day 8. Lactate dehydrogenase, cardiac troponin I (cTnI), creatine kinase MB (CK-MB), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), malondialdehyde, creatinine, and blood urea nitrogen were found to be high in the cyclophosphamide group; however, these values were reduced with apelin-13 administration. Antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, and reduced glutathione (GSH) decreased in the cyclophosphamide group, and apelin-13 increased these enzyme activities. In addition, histopathological examinations also supported the results obtained. The findings of this study showed that apelin-13 has a protective effect against cardiorenal toxicity caused by cyclophosphamide.
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Chen, Guona, Xiaoting Liang, Qian Han, et al. "Apelin-13 Pretreatment Promotes the Cardioprotective Effect of Mesenchymal Stem Cells against Myocardial Infarction by Improving Their Survival." Stem Cells International 2022 (March 21, 2022): 1–15. http://dx.doi.org/10.1155/2022/3742678.
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Although mesenchymal stem cell- (MSC-) based therapy has shown promising results for myocardial infarction (MI), low cell survival heavily limits its beneficial effects. Apelin plays an essential regulatory role in cell proliferation. This study was aimed at determining whether Apelin-13 pretreatment could improve the survival of MSCs in the ischemic heart and enhance their cardioprotective efficacy against MI. MSCs were pretreated with or without Apelin-13 for 24 hours and then exposed to serum deprivation and hypoxia (SD/H) for 48 hours. The mitochondrial morphology of MSCs was assessed by MitoTracker staining. The apoptosis of MSCs was determined by TUNEL staining. The level of mitochondrial reactive oxygen species (ROS) of MSCs was detected by Mito-Sox staining. MSCs and Apelin-13-pretreated MSCs were transplanted into the peri-infarct region in a mouse MI model. Apelin-13 pretreatment protected MSCs against SD/H-induced mitochondrial fragmentation and apoptosis. Apelin-13 pretreatment reduced ROS generation induced by SD/H in MSCs. Furthermore, Apelin-13 pretreatment enhanced the angiogenesis of MSCs under SD/H conditions. Mechanistically, Apelin-13 pretreatment inhibited SD/H-induced MSC apoptosis by downregulating mitochondrial fission via activation of the ERK pathway, and these effects were partially abrogated by ERK inhibitor U0126. Apelin-13 pretreatment promoted the survival of MSCs in the ischemic heart. Moreover, transplantation with Apelin-13-pretreated MSCs improved heart function and increased angiogenesis accompanied by decreased fibrosis compared with MSC transplantation at 28 days following MI. These findings reveal that pretreatment with Apelin-13 improves MSCs survival and enhances their therapeutic efficacy for MI. Our study provides a novel approach to improve MSC-based therapy for cardiovascular disease.
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Stupak, Aleksandra, Wojciech Kwaśniewski, Anna Goździcka-Józefiak, and Anna Kwaśniewska. "The Influence of Maternal Obesity on Cell-Free Fetal DNA and Blood Pressure Regulation in Pregnancies with Hypertensive Disorders." Medicina 57, no. 9 (2021): 962. http://dx.doi.org/10.3390/medicina57090962.
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Background and Objectives: obesity and blood pressure disorders are one of the main risk factors for antenatal, intra, postpartum, and neonatal complications. In preeclampsia (PE), the placental hypoxia leads to vascular endothelium dysfunction, cell necrosis, and apoptosis. This condition is associated with the release of free fetal DNA (cffDNA) circulating in plasma. The disturbance of the efficiency of vasodilatation and blood pressure regulation in PE can be confirmed by analyzing the apelin, salusin, and prosalusin. This study aimed to assess the influence of obesity on cffDNA, and the effectiveness of maintaining normal blood pressure in patients with preeclampsia and gestational hypertension. Material and Methods: the research material was blood serum and oral mucosa swabs, obtained from 168 patients. Pregnant women were divided into the following: a control group (C)—67 women; a gestational hypertension group (GH)—35 patients; a preeclampsia with obesity group (PE + O) (pre-gravid BMI > 30)—23 patients. The rest were lean preeclamptic women (PE)—66 patients—(pre-gravid BMI < 25 in 43 women). Results: the cffDNA was observed in 1.50% of women in the C group, in 2.45% in the GH group, but in 18.18% of lean patients with preeclampsia. The cffDNA was detected in 58% of obese pregnant women with PE. The greater the placental hypoxia was in preeclampsia, the less efficient the hypotensive mechanisms, according to an analysis of the studied adipokines. The prosalusin concentration was significantly lower in the PE group with cffDNA than in the PE group without it (p = 0.008). Apelin was higher in the PE group with cffDNA (p = 0.006) compared to other groups. The same results were also observed in the subgroup with obesity. Conclusion: in preeclamptic women, obesity seems to act as an additive factor of placental damage by means of the dysregulation of hypotensive mechanisms.
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Fibbi, Benedetta, Giada Marroncini, Laura Naldi, and Alessandro Peri. "The Yin and Yang Effect of the Apelinergic System in Oxidative Stress." International Journal of Molecular Sciences 24, no. 5 (2023): 4745. http://dx.doi.org/10.3390/ijms24054745.
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Apelin is an endogenous ligand for the G protein-coupled receptor APJ and has multiple biological activities in human tissues and organs, including the heart, blood vessels, adipose tissue, central nervous system, lungs, kidneys, and liver. This article reviews the crucial role of apelin in regulating oxidative stress-related processes by promoting prooxidant or antioxidant mechanisms. Following the binding of APJ to different active apelin isoforms and the interaction with several G proteins according to cell types, the apelin/APJ system is able to modulate different intracellular signaling pathways and biological functions, such as vascular tone, platelet aggregation and leukocytes adhesion, myocardial activity, ischemia/reperfusion injury, insulin resistance, inflammation, and cell proliferation and invasion. As a consequence of these multifaceted properties, the role of the apelinergic axis in the pathogenesis of degenerative and proliferative conditions (e.g., Alzheimer’s and Parkinson’s diseases, osteoporosis, and cancer) is currently investigated. In this view, the dual effect of the apelin/APJ system in the regulation of oxidative stress needs to be more extensively clarified, in order to identify new potential strategies and tools able to selectively modulate this axis according to the tissue-specific profile.
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Day, Robert T., Rita C. Cavaglieri, and Denis Feliers. "Apelin retards the progression of diabetic nephropathy." American Journal of Physiology-Renal Physiology 304, no. 6 (2013): F788—F800. http://dx.doi.org/10.1152/ajprenal.00306.2012.
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Apelin and its receptor APJ have pleiotropic effects in mice and humans and play a protective role in cardiovascular diseases at least partially by inhibiting oxidative stress. Our objective was to study the effect of apelin on the progression of kidney disease in mice with established type 1 diabetes. Ove26 mice with type 1 diabetes received daily subcutaneous injections of apelin for 2 or 14 wk. APJ localizes in the glomeruli and blood vessels of kidneys. Renal APJ expression was reduced in diabetic mice but increased after treatment with apelin. Apelin treatment did not affect glycemia, body weight, or blood pressure in diabetic mice. Whole kidney and glomerular hypertrophy, as well as renal inflammation, including monocyte chemoattractant protein 1 and vascular cell adhesion molecule 1 expression, NF-κB activation, and monocyte infiltration, was inhibited after short and long treatment with apelin. Apelin administration significantly reduced albuminuria at 6 mo. Short treatment with apelin was sufficient to reverse the downregulation of the antioxidant enzyme catalase. Expression of angiotensin II and angiotensin type 1 receptor (AT1) in kidneys from diabetic mice treated was not affected by apelin. These findings show for the first time that apelin exerts a protective effect on the diabetic kidney. Short administration is sufficient to reduce kidney and glomerular hypertrophy as well as renal inflammation, but prolonged treatment is required to improve albuminuria. This effect was independent of the activation of the renin angiotensin system but correlated with upregulation of the antioxidant catalase. Apelin may represent a novel tool to treat diabetic nephropathy.
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Xu, Gang, Xianming Li, Dong Yang, Shihai Wu, Dong Wu та Maosheng Yan. "Bioinformatics Study of RNA Interference on the Effect of HIF-1α on Apelin Expression in Nasopharyngeal Carcinoma Cells". Current Bioinformatics 14, № 5 (2019): 386–90. http://dx.doi.org/10.2174/1574893614666190109155825.
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Background: HIF-1α can affect the apelin expression and participates in the developments in cancers but the mechanism need to be explored further. Objective: This paper investigates apelin expression in nasopharyngeal carcinoma CNE-2 cells and its regulation by hypoxia inducible factor-1α (HIF-1α) under hypoxic conditions. Methods: CoCl2 was used to induce hypoxia in CNE-2 cells for 12h, 24h and 48h. HIF-1α small interference RNA (siRNA) was transfected into CNE-2 cells using a transient transfection method. HIF-1α and apelin mRNA levels were detected by real time PCR. Western blot was used to measure HIF-1α protein expression. The concentration of apelin in cell culture supernatant was determined by enzyme linked immunosorbent assay (ELISA). Results: HIF-1α and apelin mRNA levels and protein expression in CNE-2 cells increased gradually with increased duration of hypoxic exposure and were significantly reduced in HIF-1α siRNA transfected cells exposed to the same hypoxic conditions. Conclusion: Apelin expression is induced by hypoxia and regulated by HIF-1α in CNE-2 cells.
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Ishiguro, Koji, Makoto Yoshimoto, Masahito Tsubata, and Kinya Takagaki. "Hypotensive Effect of Sweetpotato Tops." Nippon Shokuhin Kagaku Kogaku Kaishi 54, no. 1 (2007): 45–49. http://dx.doi.org/10.3136/nskkk.54.45.
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Mlyczyńska, Ewa, Małgorzata Myszka, Patrycja Kurowska, et al. "Anti-Apoptotic Effect of Apelin in Human Placenta: Studies on BeWo Cells and Villous Explants from Third-Trimester Human Pregnancy." International Journal of Molecular Sciences 22, no. 5 (2021): 2760. http://dx.doi.org/10.3390/ijms22052760.
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Previously, we demonstrated the expression of apelin and G-protein-coupled receptor APJ in human placenta cell lines as well as its direct action on placenta cell proliferation and endocrinology. The objective of this study was to examine the effect of apelin on placenta apoptosis in BeWo cells and villous explants from the human third trimester of pregnancy. The BeWo cells and villous explants were incubated with apelin (2 and 20 ng/mL) alone or with staurosporine for 24 to 72 h. First, we analysed the dose- and time-dependent effect of apelin on the expression of apoptotic factors on the mRNA level by real-time PCR and on the protein level using Western blot. Next, we checked caspase 3 and 7 activity by Caspase-Glo 3/7, DNA fragmentation by the Cell Death Detection ELISA kit and oxygen consumption by the MitoXpress-Xtra Oxygen Consumption assay. We found that apelin increased the expression of pro-survival and decreased proapoptotic factors on mRNA and protein levels in both BeWo cells and villous explants. Additionally, apelin inhibited caspase 3 and 7 activity and DNA fragmentation in staurosporine-induced apoptosis as also attenuated oxidative stress by increasing extracellular oxygen consumption. The antiapoptotic effect of apelin in BeWo cells was mediated by the APJ receptor and mitogen-activated protein kinase (ERK1/2/MAP3/1) and protein kinase B (AKT). The obtained results showed the antiapoptotic effect of apelin on trophoblast cells, suggesting its participation in the development of the placenta.
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Wang, Chen, Jun-Feng Du, Feng Wu, and Hai-Chang Wang. "Apelin decreases the SR Ca2+ content but enhances the amplitude of [Ca2+]i transient and contractions during twitches in isolated rat cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 6 (2008): H2540—H2546. http://dx.doi.org/10.1152/ajpheart.00046.2008.
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Apelin has been reported to have a positive inotropic action in the isolated rat heart. However, the effect of apelin on sarcoplasmic reticulum (SR) Ca2+ content and its influence on intracellular Ca2+ transient during excitation-contraction coupling remains poorly understood. In the present study, we determined the effect of apelin on Ca2+ transient and contractions in isolated rat cardiomyocytes. When compared with control, treatment with apelin caused a 55.7 ± 13.9% increase in sarcomere fraction shortening and a 43.6 ± 4.56% increase in amplitude of electrical-stimulated intracellular Ca2+ concentration (E[Ca2+]i) transients ( n = 14, P < 0.05). But SR Ca2+ content measured by caffeine-induced [Ca2+]i (C[Ca2+]i) transient was decreased 8.41 ± 0.92% in response to apelin ( n = 14, P < 0.05). Na+/Ca2+ exchanger (NCX) function was increased since half-decay time of C[Ca2+]i was decreased 16.22 ± 1.36% in response to apelin. Sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) activity was also increased by apelin. These responses can be partially or completely blocked by chelerythrine chloride, a PKC inhibitor. In addition, to confirm our data, we used indo-1 as another Ca2+ indicator and rapid cooling as another way to measure SR Ca2+ content, and we observed similar results. So we conclude that apelin has a positive inotropic effect on isolated myocytes, and increased amplitude of E[Ca2+]i is at least partially involved in the mechanism. NCX function and SERCA activity are increased by apelin, and the SR Ca2+ content is decreased by apelin during twitches. PKC played an important role in these signaling mechanisms.
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Berezin, Alexander A., Ivan M. Fushtey, and Alexander E. Berezin. "The Effect of SGLT2 Inhibitor Dapagliflozin on Serum Levels of Apelin in T2DM Patients with Heart Failure." Biomedicines 10, no. 7 (2022): 1751. http://dx.doi.org/10.3390/biomedicines10071751.
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Apelin is a multifunctional peptide that plays a pivotal role in cardiac remodeling and HF manifestation because of counteracting angiotensin-II. We hypothesized that positive influence of sodium-glucose co-transporter-2 (SGLT2) inhibitor on cardiac function in T2DM patients with HF might be mediated by apelin and that its levels seem to be a target of management. A total of 153 type 2 diabetes mellitus (T2DM) patients with II/III HF NYHA class and average left ventricular (LV) ejection fraction (EF) of 46% have been enrolled and treated with dapagliflosin. The serum levels of apelin and N-terminal brain natriuretic pro-peptide (NT-proBNP) were measured at baseline and over a 6-month period of dapagliflosin administration. We noticed that administration of dapagliflozin was associated with a significant increase in apelin levels of up to 18.3% and a decrease in NT-proBNP of up to 41.0%. Multivariate logistic regression showed that relative changes of LVEF, LA volume index, and early diastolic blood filling to longitudinal strain ratio were strongly associated with the levels of apelin, whereas NT-proBNP exhibited a borderline significance in this matter. In conclusion, dapagiflosin exerted a positive impact on echocardiographic parameters in close association with an increase in serum apelin levels, which could be a surrogate target for HF management.
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Kurowska, Patrycja, Alix Barbe, Marta Różycka, Justyna Chmielińska, Joelle Dupont, and Agnieszka Rak. "Apelin in Reproductive Physiology and Pathology of Different Species: A Critical Review." International Journal of Endocrinology 2018 (June 6, 2018): 1–12. http://dx.doi.org/10.1155/2018/9170480.
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Apelin has been isolated from the bovine stomach extracts as an endogenous ligand of the previously orphan receptor APJ. Expression of the apelinergic system (apelin and APJ) was described in many organs where pleiotropic effects like regulation of food intake, body weight, or cardiovascular and immune function were described. Recent studies have shown that apelin also plays an important role in the regulation of female and male reproduction. Some data showed that the gene and protein of apelin/APJ are expressed in the hypothalamic-pituitary-gonad (HPG) axis tissue. Thus, apelin is synthesized locally in the hypothalamus, pituitary, ovaries, and testis of many species and has autocrine and/or paracrine effects. Most research indicates that apelin has an inhibitory effect on gonadotropin secretion and participates in the direct regulation of steroidogenesis, cell proliferation, and apoptosis in gonads. The article summarizes also results of a series of recent studies on the effect of apelin on reproduction pathology, like polycystic ovarian syndrome, endometriosis, and ovarian cancer. Many of these pathologies are still in critical need of therapeutic intervention, and recent studies have found that apelin can be targets in reproductive pathological states.
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Bülbül, Mehmet, V. Nimet İzgüt-Uysal, Osman Sinen, İlknur Birsen, and Gamze Tanrıöver. "Central apelin mediates stress-induced gastrointestinal motor dysfunction in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 310, no. 4 (2016): G249—G261. http://dx.doi.org/10.1152/ajpgi.00145.2015.
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Apelin, an endogenous ligand for APJ receptor, has been reported to be upregulated in paraventricular nucleus (PVN) following stress. Central apelin is known to stimulate release of corticotropin-releasing factor (CRF) via APJ receptor. We tested the hypothesis that stress-induced gastrointestinal (GI) dysfunction is mediated by central apelin. We also assessed the effect of exogenous apelin on GI motility under nonstressed (NS) conditions in conscious rats. Prior to solid gastric emptying (GE) and colon transit (CT) measurements, APJ receptor antagonist F13A was centrally administered under NS conditions and following acute stress (AS), chronic homotypic stress (CHS), and chronic heterotypic stress (CHeS). Plasma corticosterone was assayed. Strain gage transducers were implanted on serosal surfaces of antrum and distal colon to record postprandial motility. Stress exposure induced coexpression of c-Fos and apelin in hypothalamic PVN. Enhanced hypothalamic apelin and CRF levels in microdialysates were detected following AS and CHeS, which were negatively and positively correlated with GE and CT, respectively. Central F13A administration abolished delayed GE and accelerated CT induced by AS and CHeS. Central apelin-13 administration increased the plasma corticosterone and inhibited GE and CT by attenuating antral and colonic contractions. The inhibitory effect elicited by apelin-13 was abolished by central pretreatment of CRF antagonist CRF9–41 in antrum, but not in distal colon. Central endogenous apelin mediates stress-induced changes in gastric and colonic motor functions through APJ receptor. The inhibitory effects of central exogenous apelin-13 on GI motility appear to be partly CRF dependent. Apelin-13 inhibits colon motor functions through a CRF-independent pathway.
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Rastaldo, Raffaella, Sandra Cappello, Anna Folino, and Gianni Losano. "Effect of Apelin-Apelin Receptor System in Postischaemic Myocardial Protection: A Pharmacological Postconditioning Tool?" Antioxidants & Redox Signaling 14, no. 5 (2011): 909–22. http://dx.doi.org/10.1089/ars.2010.3355.
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Jiang, He, Xiao-Ping Ye, Zhong-Yin Yang, et al. "Aldosterone directly affects apelin expression and secretion in adipocytes." Journal of Molecular Endocrinology 51, no. 1 (2013): 37–48. http://dx.doi.org/10.1530/jme-13-0025.
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There is a high incidence of metabolic syndrome among patients with primary aldosteronism (PA), which has recently been associated with an unfavorable cardiometabolic profile. However, the underlying mechanisms have not been clarified in detail. Characterizing aldosterone (Ald) target genes in adipocytes will help us to elucidate the deleterious effects associated with excess Ald. Apelin, a novel adipokine, exerts beneficial effects on obesity-associated disorders and cardiovascular homeostasis. The objective of this study was to investigate the effects of high Ald levels on apelin expression and secretion and the underlying mechanisms involved in adipocytes. In vivo, a single-dose Ald injection acutely decreased apelin serum levels and adipose tissue apelin production, which demonstrates a clear inverse relationship between the levels of plasma Ald and plasma apelin. Experiments using 3T3-L1 adipocytes showed that Ald decreased apelin expression and secretion in a time- and dose-dependent manner. This effect was reversed by glucocorticoid receptor (GR) antagonists or GR (NR3C1) knockdown; furthermore, putative HREs were identified in the apelin promoter. Subsequently, we verified that both glucocorticoids and mineralocorticoids regulated apelin expression through GR activation, although no synergistic effect was observed. Additionally, detailed potential mechanisms involved a p38 MAPK signaling pathway. In conclusion, our findings strengthen the fact that there is a direct interaction between Ald and apelin in adipocytes, which has important implications for hyperaldosteronism or PA-associated cardiometabolic syndrome and hoists apelin on the list of potent therapeutic targets for PA.
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Hamza, Reham Z., Abdel Aziz A. Diab, Mansour H. Zahra, Ali K. Asalah, Mai S. Attia, and Suzan MM Moursi. "Ameliorative effect of apelin-13 against renal complications in L-NAME-induced preeclampsia in rats." PeerJ 9 (March 31, 2021): e11110. http://dx.doi.org/10.7717/peerj.11110.
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Pre-eclampsia (PE) accompanying acute liver and kidney injury has remained a master cause of both fetal and maternal mortality and morbidity. Vasoactive mediators, oxidative stress and inflammatory imbalanceshave an important role in PE pathogenesis. Apelin is an adipokine that improves endothelial dysfunction; has anti-inflammatory and antioxidant effects; moreover, its level reduced during PE. This study aimed to explore the effects of apelin-13 administration on preeclampsia-associated renal dysfunction and proteinuria. Thirty-three pregnant female rats were divided into three groups; group: 1 (normal pregnant rats), group: 2 (preeclamptic rats); where rats were injected subcutaneously with 75 mg L-NAME/ kg body weight/day beginning from 9th to 20th day of pregnancy andgroup 3 (apelin-13 treated preeclamptic rats); In which L-NAME-induced preeclamptic rats were subcutaneously injected with 6 × 10−8 mol apelin-13/kg body weight/twice daily starting from 6th to 20th day of pregnancy. In all groups, mean arterial blood pressure, total urine protein, serum urea, creatinine, nitric oxide (NO), endothelin-1 (ET-1), interleukin–6 (IL-6) and malondialdhyde (MDA) were measured. Histopathological examination of kidney tissues was also done. preeclamptic rats showed significantly increased mean arterial blood pressure, total urine proteins, serum urea, creatinine, ET-1, IL-6, and MDA, but revealed a significantly decreased serum NO level. On the other hand, apelin treatment significantly improved these parameters together with amelioration of kidney histoarchitecture in the treated group. In conclusion, apelin may be a potentially curative candidate for prohibiting kidney damage and have a therapeutic benefit in PE rat models.
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Chen, Li, Yong Tao, Jing Feng, and Yan Rong Jiang. "Apelin Protects Primary Rat Retinal Pericytes from Chemical Hypoxia-Induced Apoptosis." Journal of Ophthalmology 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/186946.
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Pericytes are a population of cells that participate in normal vessel architecture and regulate permeability. Apelin, as the endogenous ligand of G protein-coupled receptor APJ, participates in a number of physiological and pathological processes. To date, the effect of apelin on pericyte is not clear. Our study aimed to investigate the potential protection mechanisms of apelin, with regard to primary rat retinal pericytes under hypoxia. Immunofluorescence staining revealed that pericytes colocalized with APJ in the fibrovascular membranes dissected from proliferative diabetic retinopathy patients. In thein vitrostudies, we first demonstrated that the expression of apelin/APJ was upregulated in pericytes under hypoxia, and apelin increased pericytes proliferation and migration. Moreover, knockdown of apelin in pericyte was achieved via lentivirus-mediated RNA interference. After the inhibition of apelin, pericytes proliferation was inhibited significantly in hypoxia culture condition. Furthermore, exogenous recombinant apelin effectively prevented hypoxia-induced apoptosis through downregulating active-caspase 3 expression and increasing the ratio of B cell lymphoma-2 (Bcl-2)/Bcl-2 associated X protein (Bax) in pericytes. These results suggest that apelin suppressed hypoxia-induced pericytes injury, which indicated that apelin could be a potential therapeutic target for retinal angiogenic diseases.
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Tobin, Vicky A., Philip M. Bull, Sathya Arunachalam, Anne-Marie O'Carroll, Yoichi Ueta, and Mike Ludwig. "The Effects of Apelin on the Electrical Activity of Hypothalamic Magnocellular Vasopressin and Oxytocin Neurons and Somatodendritic Peptide Release." Endocrinology 149, no. 12 (2008): 6136–45. http://dx.doi.org/10.1210/en.2008-0178.
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Apelin, a novel peptide originally isolated from bovine stomach tissue extracts, is widely but selectively distributed throughout the nervous system. Vasopressin and oxytocin are synthesized in the magnocellular neurons of the hypothalamic supraoptic nucleus (SON) and paraventricular nucleus, which are apelin-rich regions in the central nervous system. We made extracellular electrophysiological recordings from the transpharyngeally exposed SON of urethane-anaesthetized rats to assess the role of apelin in the control of the firing activity of identified magnocellular vasopressin and oxytocin neurons in vivo. Apelin-13 administration onto SON neurons via microdialysis revealed cell-specific responses; apelin-13 increased the firing rates of vasopressin cells but had no effect on the firing rate of oxytocin neurons. A direct excitatory effect of apelin-13 on vasopressin cell activity is also supported by our in vitro studies showing depolarization of membrane potential and increase in action potential firing. To assess the effects of apelin-13 on somatodendritic peptide release, we used in vitro release studies from SON explants in combination with highly sensitive and specific RIA. Apelin-13 decreases basal (by 78%; P &lt; 0.05; n = 6) and potassium-stimulated (by 57%; P &lt; 0.05; n = 6) vasopressin release but had no effect on somatodendritic oxytocin release. Taken together, our data suggest a local autocrine feedback action of apelin on magnocellular vasopressin neurons. Furthermore, these data show a marked dissociation between axonal and dendritic vasopressin release with a decrease in somatodendritic release but an increase in electrical activity at the cell bodies, indicating that release from these two compartments can be regulated wholly independently.
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Respekta, Natalia, Karolina Pich, Monika Dawid, Ewa Mlyczyńska, Patrycja Kurowska, and Agnieszka Rak. "The Apelinergic System: Apelin, ELABELA, and APJ Action on Cell Apoptosis: Anti-Apoptotic or Pro-Apoptotic Effect?" Cells 12, no. 1 (2022): 150. http://dx.doi.org/10.3390/cells12010150.
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The apelinergic system comprises two peptide ligands, apelin and ELABELA, and their cognate G-protein-coupled receptor, the apelin receptor APJ. Apelin is a peptide that was isolated from bovine stomach extracts; the distribution of the four main active forms, apelin-36, -17, -13, and pyr-apelin-13 differs between tissues. The mature form of ELABELA-32 can be transformed into forms called ELABELA-11 or -21. The biological function of the apelinergic system is multifaceted, and includes the regulation of angiogenesis, body fluid homeostasis, energy metabolism, and functioning of the cardiovascular, nervous, respiratory, digestive, and reproductive systems. This review summarises the mechanism of the apelinergic system in cell apoptosis. Depending on the cell/tissue, the apelinergic system modulates cell apoptosis by activating various signalling pathways, including phosphoinositide 3-kinase (PI3K), extracellular signal-regulated protein kinase (ERK1/2), protein kinase B (AKT), 5’AMP-activated protein kinase(AMPK), and protein kinase A (PKA). Apoptosis is critically important during various developmental processes, and any dysfunction leads to pathological conditions such as cancer, autoimmune diseases, and developmental defects. The purpose of this review is to present data that suggest a significant role of the apelinergic system as a potential agent in various therapies.
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Shpakov, A. O., and K. V. Derkach. "The Role of Apelin in the Functioning of the Reproductive System." Acta Biomedica Scientifica 4, no. 3 (2019): 7–17. http://dx.doi.org/10.29413/abs.2019-4.3.1.
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Adipokine apelin through the apelin receptors activates a wide range of signaling cascades in the target cells and controls their growth, differentiation, apoptosis, and energy metabolism. In the recent years, the evidence has been obtained that all components of the hypothalamic-pituitary-gonad axis, in which apelin and its receptor are expressed, are targets of apelin. In the hypothalamus, apelin modulates the activity of the melanocortin and ghrelin systems and indirectly affects the production of gonadoliberin. In the ovaries, it controls the growth and maturation of the follicles, stimulates the angiogenesis, and affects the basal and stimulated by the other factors steroidogenic activity in follicular cells. The changes in the apelin signaling system are closely associated with dysfunctions of the female reproductive system, such as polycystic ovary syndrome, endometriosis, and cancer. Information on the regulation of the male reproductive system by apelin is limited to animal studies showing the effect of apelin on the hypothalamic components of the gonad axis. The participation of apelin in the regulation of the reproductive system opens up the broad opportunities for the development of new approaches for the correction of abnormalities in this system and for the treatment of infertility.
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Akbari, Hamed, Mahnaz Hosseini-Bensenjan, Sarvenaz Salahi, et al. "Apelin and its ratio to lipid factors are associated with cardiovascular diseases: A systematic review and meta-analysis." PLOS ONE 17, no. 8 (2022): e0271899. http://dx.doi.org/10.1371/journal.pone.0271899.
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Background The present systematic review and meta-analysis aimed to ascertain if the circulating levels of apelin, as an important regulator of the cardiovascular homeostasis, differ in patients with cardiovascular diseases (CVDs) and controls. Methods A comprehensive search was performed in electronic databases including PubMed, Scopus, EMBASE, and Web of Science to identify the studies addressing apelin in CVD up to April 5, 2021. Due to the presence of different units to measure the circulating levels of apelin across the included studies, they expressed the standardized mean difference (SMD) and their 95% confidence interval (CI) as summary effect size. A random-effects model comprising DerSimonian and Laird method was used to pool SMDs. Results Twenty-four articles (30 studies) comprised of 1793 cases and 1416 controls were included. Pooled results obtained through random-effects model indicated that apelin concentrations in the cases’ blood samples were significantly lower than those of the control groups (SMD = -0.72, 95% CI: -1.25, -0.18, P = 0.009; I2 = 97.3%, P<0.001). New combined biomarkers showed a significant decrease in SMD of apelin/high-density lipoprotein cholesterol (apelin/HDL-C) ratio [-5.17; 95% CI, -8.72, -1.63, P = 0.000; I2 = 99.0%], apelin/low-density lipoprotein cholesterol (apelin/LDL-C) ratio [-4.31; 95% CI, -6.08, -2.55, P = 0.000; I2 = 98.0%] and apelin/total cholesterol (apelin/TC) ratio [-17.30; 95% CI, -22.85, -11.76, P = 0.000; I2 = 99.1%]. However, no significant differences were found in the SMD of apelin/triacylglycerol (apelin/TG) ratio in cases with CVDs compared to the control group [-2.96; 95% CI, -7.41, 1.49, P = 0.000; I2 = 99.2%]. Conclusion The association of apelin with CVDs is different based on the region and disease subtypes. These findings account for the possible usefulness of apelin as an additional biomarker in the diagnosis of CVD in diabetic patients and in the diagnosis of patients with CAD. Moreover, apelin/HDL-c, apelin/LDL-c, and apelin/TC ratios could be offered as diagnostic markers for CVD.
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Bodineau, Laurence, Christopher Taveau, Hong-Hanh Lê Quan Sang, et al. "Data Supporting a New Physiological Role for Brain Apelin in the Regulation of Hypothalamic Oxytocin Neurons in Lactating Rats." Endocrinology 152, no. 9 (2011): 3492–503. http://dx.doi.org/10.1210/en.2011-0206.
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Apelin is a bioactive peptide identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ in 1998. The present data show that apelin modulates the activity of magnocellular and parvocellular oxytocin (OXY) neurons in the lactating rat. A combination of in situ hybridization and immunohistochemistry demonstrated the presence of apelin receptor mRNA in hypothalamic OXY neurons. Double immunofluorescence labeling then revealed the colocalization of apelin with OXY in about 20% of the hypothalamic OXY-positive neurons. Intracerebroventricular apelin administration inhibited the activity of magnocellular and parvocellular OXY neurons, as shown by measuring the c-fos expression in OXY neurons or by direct electrophysiological measurements of the electrical activity of these neurons. This effect was correlated with a decrease in the amount of milk ejected. Thus, apelin inhibits the activity of OXY neurons through a direct action on apelin receptors expressed by these neurons in an autocrine and paracrine manner. In conclusion, these findings highlight the inhibitory role of apelin as an autocrine/paracrine peptide acting on OXY neurons during breastfeeding.
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Xu, Gang, Xianming Li, Shihai Wu, Dong Yang, and Mao Sheng Yan. "Biostatistical Relationship Between Apelin Expression and Radiosensitization in Nasopharyngeal Carcinoma Cells Based on Flow Cytometry and Cell Imaging." Journal of Medical Imaging and Health Informatics 9, no. 8 (2019): 1575–82. http://dx.doi.org/10.1166/jmihi.2019.2765.
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Objective: To explore the biostatistical relationship between Apelin expression and radiosensitization in nasopharyngeal carcinoma (NPC) cells. Methods: The main operation of the experiment on NPC cells 6-10B and HNE2 include: colony formation, flow cytometry for radiotherapy, detection of cell proliferation according to the results of radiotherapy, protein immunoblotting for cells, detection of the effect of Apelin on the expression of hormones in cells by Western Blot method, immunofluorescence assay, electrophoresis, transmembrane closure, incubation of anti-cancer cells. The effects of Apelin on NPC cells were obtained by biostatistical analysis. Cells were scanned by a scanning electron microscope, the anisotropic analysis algorithm was used to analyze and compare the results of cell radiotherapy. Results: Apelin-13 inhibits the proliferation of NPC cells 6-10B and HNE2. Moreover, Apelin-13 can induce the overexpression of Cyclin D1 in NPC cells and promote the proliferation of NPC cells and inhibition of Caspase 3 expression and apoptosis of NPC cells. Apelin also has a significant effect on radiosensitization of NPC cells. Conclusion: Apelin controls the expression of Cyclin D1 and Casepase 3 cytokines. It can increase the apoptotic degree of NPC cells, inhibit the proliferation of NPC cells, and improve the radiosensitivity of NPC cells.
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Vitale, Emanuela, Rachele Rosso, Marco Lo Iacono, Caterina Cristallini, Claudia Giachino, and Raffaella Rastaldo. "Apelin-13 Increases Functional Connexin-43 through Autophagy Inhibition via AKT/mTOR Pathway in the Non-Myocytic Cell Population of the Heart." International Journal of Molecular Sciences 23, no. 21 (2022): 13073. http://dx.doi.org/10.3390/ijms232113073.
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Studies have shown a link between the downregulation of connexin 43 (Cx43), the predominant isoform in cardiac gap junctions, and high susceptibility to cardiac arrhythmias and cardiomyocyte death. Non-myocytic cells (NMCs), the most abundant component of the heart, exert multiple cardiac functions and represent an important therapeutic target for diseased cardiac tissue. A few studies have investigated the effect of Apelin-13, an endogenous peptide with a key role in various cardiovascular functions, on Cx43 expression in cardiomyocytes. However, it remained unknown whether Apelin-13 influences Cx43 expression in NMCs. Here, we found that in NMCs, Cx43 protein expression increased after Apelin-13 treatment (100 nM for 48 h). Furthermore, dye transfer assays proved that Apelin-13-treated NMCs had a greater ability to communicate with surrounding cardiomyocytes, and this effect was abrogated by carbenoxolone, a gap junction inhibitor. Interestingly, we showed that Apelin-13 increased Cx43 through autophagy inhibition, as proved by the upregulation of p62 and LC3I, acting as 3-MA, a well-known autophagy inhibitor. In addition, Apelin-13-induced AKT and mTOR phosphorylation was abolished by LY294002 and rapamycin inhibitors resulting in Cx43 increased suppression. These results open the possibility of targeting gap junctions in NMCs with Apelin-13 as an exciting therapeutic approach with great potential.
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SUGIYAMA, Keikichi, Koji TAKADA, Makoto EGAWA, Ikuo YAMAMOTO, Hiromu ONZUKA, and Kenkichi ÔBA. "Hypotensive effect of fish protein hydrolysate." Journal of the agricultural chemical society of Japan 65, no. 1 (1991): 35–43. http://dx.doi.org/10.1271/nogeikagaku1924.65.35.
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Domaingue, Charles M., and Daryl H. Nye. "Hypotensive Effect of Mannitol Administered Rapidly." Anaesthesia and Intensive Care 13, no. 2 (1985): 134–36. http://dx.doi.org/10.1177/0310057x8501300204.
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Henning, M., та P. A. Zwieten. "Central Hypotensive Effect of α-methyldopa". Acta Pharmacologica et Toxicologica 25, S4 (2009): 25. http://dx.doi.org/10.1111/j.1600-0773.1967.tb03015.x.
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Villar, A., M. C. Terencio, and M. Paya. "Hypotensive effect of Rhamnus lycioides extracts." Journal of Ethnopharmacology 16, no. 2-3 (1986): 269–73. http://dx.doi.org/10.1016/0378-8741(86)90093-0.
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Sheikh, Ahmad Y., Hyung J. Chun, Alexander J. Glassford, et al. "In vivo genetic profiling and cellular localization of apelin reveals a hypoxia-sensitive, endothelial-centered pathway activated in ischemic heart failure." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 1 (2008): H88—H98. http://dx.doi.org/10.1152/ajpheart.00935.2007.
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Signaling by the peptide ligand apelin and its cognate G protein-coupled receptor APJ has a potent inotropic effect on cardiac contractility and modulates systemic vascular resistance through nitric oxide-dependent signaling. In addition, there is evidence for counterregulation of the angiotensin and vasopressin pathways. Regulatory stimuli of the apelin-APJ pathway are of obvious importance but remain to be elucidated. To better understand the physiological response of apelin-APJ to disease states such as heart failure and to elucidate the mechanism by which such a response might occur, we have used the murine model of left anterior descending coronary artery ligation-induced ischemic cardiac failure. To identify the key cells responsible for modulation and production of apelin in vivo, we have created a novel apelin-lacZ reporter mouse. Data from these studies demonstrate that apelin and APJ are upregulated in the heart and skeletal muscle following myocardial injury and suggest that apelin expression remains restricted to the endothelium. In cardiac failure, endothelial apelin expression correlates with other hypoxia-responsive genes, and in healthy animals both apelin and APJ are markedly upregulated in various tissues following systemic hypoxic exposure. Experiments with cultured endothelial cells in vitro show apelin mRNA and protein levels to be increased by hypoxia, through a hypoxia-inducible factor-mediated pathway. These studies suggest that apelin-expressing endothelial cells respond to conditions associated with heart failure, possibly including local tissue hypoxia, and modulate apelin-APJ expression to regulate cardiovascular homeostasis. The apelin-APJ pathway may thus provide a mechanism for systemic endothelial monitoring of tissue perfusion and adaptive regulation of cardiovascular function.
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Mishra, Aastha, Samantha Kohli, Sanchi Dua, Tashi Thinlas, Ghulam Mohammad, and M. A. Qadar Pasha. "Genetic differences and aberrant methylation in the apelin system predict the risk of high-altitude pulmonary edema." Proceedings of the National Academy of Sciences 112, no. 19 (2015): 6134–39. http://dx.doi.org/10.1073/pnas.1422759112.
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Hypoxia-inducible factor stimulates the expression of apelin, a potent vasodilator, in response to reduced blood arterial oxygen saturation. However, aberrations in the apelin system impair pulmonary vascular function, potentially resulting in the development of high-altitude (HA)-related disorders. This study aimed to elucidate the genetic and epigenetic regulation of apelin, apelin receptor (APLNR), and endothelial nitric oxide synthase (NOS3) in HA adaptation and HA pulmonary edema (HAPE). A genome-wide association study and sequencing identified variants of apelin, APLNR, and NOS3 that were validated in a larger sample size of HAPE-patients (HAPE-p), HAPE-free controls (HAPE-f), and healthy highland natives (HLs). Apelin-13 and nitrite levels and apelin and NOS3 expression were down-regulated in HAPE-p (P < 0.001). Among the several studied polymorphisms, apelin rs3761581, rs2235312, and rs3115757; APLNR rs11544374 and rs2282623; and NOS3 4b/4a, rs1799983, and rs7830 were associated with HAPE (P < 0.03). The risk allele rs3761581G was associated with a 58.6% reduction in gene expression (P = 0.017), and the risk alleles rs3761581G and rs2235312T were associated with low levels of apelin-13 and nitrite (P < 0.05). The latter two levels decreased further when both of these risk alleles were present in the patients (P < 0.05). Methylation of the apelin CpG island was significantly higher in HAPE-p at 11.92% than in HAPE-f and HLs at ≤7.1% (P < 0.05). Moreover, the methylation effect was 9% stronger in the 5′ UTR and was associated with decreased apelin expression and apelin-13 levels. The rs3761581 and rs2235312 polymorphisms and methylation of the CpG island influence the expression of apelin in HAPE.
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Han, Xue, Dong-Liang Zhang, Dao-Xin Yin, Qi-Dong Zhang, and Wen-Hu Liu. "Apelin-13 deteriorates hypertension in rats after damage of the vascular endothelium by ADMA." Canadian Journal of Physiology and Pharmacology 91, no. 9 (2013): 708–14. http://dx.doi.org/10.1139/cjpp-2013-0046.
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Asymmetric dimethylarginine (ADMA) is a risk factor for endothelial dysfunction. The polypeptide apelin has biphasic effects on blood vessels in vivo and in vitro. We investigated the effect of apelin-13 on ADMA-damaged vessels. Rats were divided among ADMA-treated and control groups, which were treated with ADMA (10 mg·(kg body mass)−1·day−1) or saline, respectively, for 4 weeks. Systolic blood pressure (SBP) was measured before and after the injection of apelin-13. The ultrastructure of endothelial cells in caudal arteries was examined using transmission electron microscopy. The reactivities of isolated caudal artery rings were observed after exposure to apelin-13, and myosin light chain (MLC) phosphorylation was assessed by immunohistochemistry in rings treated with or without apelin-13. ADMA induced hypertension and endothelial dysfunction. After injection of apelin-13, SBP declined in the control group but was elevated in the ADMA-treated group. In vitro, apelin-13 caused relaxation in rings in the control group, but it contracted rings in the ADMA-treated group. Apelin-13 promoted MLC phosphorylation in vascular smooth muscle cells (VSMCs) in the ADMA group. These results indicate that apelin-13 might pass through ADMA-damaged endothelium and act on VSMCs to increase MLC phosphorylation, thus contributing to vasoconstriction and exacerbating hypertension.
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Wang, Sha, Guoying Gao, Yiwei He, Qiong Li, Zhan Li та Guoxiang Tong. "Amidation-Modified Apelin-13 Regulates PPARγ and Perilipin to Inhibit Adipogenic Differentiation and Promote Lipolysis". Bioinorganic Chemistry and Applications 2021 (7 травня 2021): 1–9. http://dx.doi.org/10.1155/2021/3594630.
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With the adjustment of human diet and lifestyle changes, the prevalence of obesity is increasing year by year. Obesity is closely related to the excessive accumulation of white adipose tissue (WAT), which can synthesize and secrete a variety of adipokines. Apelin is a biologically active peptide in the adipokines family. Past studies have shown that apelin plays an important regulatory role in the pathogenesis and pathophysiology of diseases such as the cardiovascular system, respiratory system, digestive system, nervous system, and endocrine system. Apelin is also closely related to diabetes and obesity. Therefore, we anticipate that apelin-13 has an effect on lipometabolism and intend to explore the effect of apelin-13 on lipometabolism at the cellular and animal levels. In in vitro experiments, amidation-modified apelin-13 can significantly reduce the lipid content; TG content; and the expression of PPARγ, perilipin mRNA, and protein in adipocytes. Animal experiments also show that amidation modification apelin-13 can improve the abnormal biochemical indicators of diet-induced obesity (DOI) rats and can reduce the average diameter of adipocytes in adipose tissue, the concentration of glycerol, and the expression of PPARγ and perilipin mRNA and protein. Our results show that apelin-13 can affect the metabolism of adipose tissue, inhibit adipogenic differentiation of adipocytes, promote lipolysis, and thereby improve obesity. The mechanism may be regulating the expression of PPARγ to inhibit adipogenic differentiation and regulating the expression of perilipin to promote lipolysis. This study helps us understand the role of apelin-13 in adipose tissue and provide a basis for the elucidation of the regulation mechanism of lipometabolism and the development of antiobesity drugs.
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Xu, Shu, Jian Zhang, Yin-li Xu, Hai-bo Wu, Xiao-dong Xue, and Hui-shan Wang. "Relationship between Angiotensin Converting Enzyme, Apelin, and New-Onset Atrial Fibrillation after Off-Pump Coronary Artery Bypass Grafting." BioMed Research International 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/7951793.
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It has been shown that inflammation and oxidative stress are important factors in postoperative atrial fibrillation (POAF). Angiotensin converting enzyme (ACE) and apelin have a close relationship with inflammation and oxidative stress. The effect of ACE and apelin on POAF after off-pump coronary artery bypass grafting (OPCABG) remains a question. The concentrations of serum ACE, angiotensin II (Ang II), apelin, bradykinin (BK), malondialdehyde (MDA), and C reactive protein (CRP) were measured in the perioperative period of OPCABG. The levels of serum ACE in the POAF group were higher than in the no POAF group both preoperatively and postoperatively. Apelin in the POAF group was lower than in the no POAF group. There was a correlation between serum ACE and apelin. Postoperatively, CRP and MDA in the POAF group were higher than in the no POAF group; however, there was no difference before the operation. Preoperative ACE and apelin were both significant and independent risk factors for POAF. In conclusion, the high ACE and low apelin preoperatively led to CRP and MDA being increased postoperatively, which was probably associated with POAF after OPCABG. Apelin may be a new predictor for POAF.
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Mousa J. Humesh, AbduL-Monaim H.M. AL-Samarraie, and Zainab A.L. AL-Samarraie. "Apelin Levels and its Relationship with a Number of Electrolytes in Patients with Myocardial Infarction." Tikrit Journal of Pure Science 23, no. 3 (2018): 16–22. http://dx.doi.org/10.25130/tjps.v23i3.495.
Full textAbstract:
The study aimed to determine the effect of the lack of Apelin peptide and its relation to the development and severity of coronary atherosclerosis and to prove its association with acute myocardial infarction and the positive effect when increasing its concentration in the body and protect it from various diseases. The study included 70 patients of different ages infected with myocardial infarction, both high blood pressure and diabetes, were significantly presented in the group of patients in this study and were compared with control group, which included 35 samples of healthy people. The study showed that there was a significant decrease (P≤0.05) in Apelin concentration in people who suffered from myocardial infarction compared with the control group, which was their Apelin concentrations within the normal rates, there was a significant decrease (P≤ 0.05) in the concentration of Apelin with males and females who suffered from myocardial infarction compared with males and females in control group, which was within normal concentrations that existed in the blood, parameters were measured the concentrations of Apelin and the results of study as follows: There was a significant decrease (P≤0.05) in the concentration of sodium, potassium, chloride and magnesium ions in patients with myocardial infarction compared with the control group. The concentrations of electrolytes in the sera of males and females were significantly decreases (P≤0.05) in regard to sodium, potassium and chloride ions in males and females patients compared to control group, while there were no significant differences (P≤0.05) in the concentration of magnesium between males and females of patients and control group. The correlation of sodium, potassium, magnesium and chloride ions with the concentration of the Apelin was positive. It rises continuously with elevation in the concentration of the Apelin and decrease in the concentration of Apelin. This has a positive effect on myocardial function and improve its function.
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Marczewski, Kamil, Natalia Gospodarczyk, Alicja Gospodarczyk, Michał Widuch, and Michał Tkocz. "APELIN IN HEART FAILURE." Wiadomości Lekarskie 75, no. 10 (2022): 2501–6. http://dx.doi.org/10.36740/wlek202210130.
Full textAbstract:
Apelin is a biologically active protein encoded by the APLN gene. It was first isolated in 1998 as a ligand for the APJ receptor. It exists in several isoforms differing in polypeptide chain length and biological activity. It is secreted by white adipose tissue, and its expression has been identified in many body tissues, including the cardiovascular system, kidneys, lungs, CNS (especially the hypothalamus, suprachiasmatic and ventricular nuclei), skeletal muscle, mammary glands, adrenal glands, ovaries, stomach, liver cells, placenta, and breast milk. However, the highest concentrations were observed in the endocardium and endothelium of vascular smooth muscle cells. In myocardial tissue, apelin has a positive inotropic effect and exerts an opposing effect to the RAA (renin-angiotensin-aldosterone) system, lowering blood pressure. Therefore, its positive role in early stages of heart failure, in patients with hypertension and ischemic heart disease is emphasized. The synthesis and secretion of apelin by adipocytes makes it possible to classify this peptide as an adipokine. Therefore, its production in adipose tissue is enhanced in obesity. Furthermore, apelin has been shown to increase cellular sensitivity to insulin and improve glucose tolerance in the onset of type 2 diabetes, and therefore appears to play a significant role in the pathogenesis of metabolic disease. An accurate assessment of the importance of apelin in cardiovascular disease requires further studies, which may contribute to the use of apelin in the treatment of heart failure.
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Tune, Johnathan D., Hana E. Baker, Zachary Berwick, et al. "Distinct hemodynamic responses to (pyr)apelin-13 in large animal models." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 4 (2020): H747—H755. http://dx.doi.org/10.1152/ajpheart.00365.2019.
Full textAbstract:
This study tested the hypothesis that (pyr)apelin-13 dose-dependently augments myocardial contractility and coronary blood flow, irrespective of changes in systemic hemodynamics. Acute effects of intravenous (pyr)apelin-13 administration (10 to 1,000 nM) on blood pressure, heart rate, left ventricular pressure and volume, and coronary parameters were measured in dogs and pigs. Administration of (pyr)apelin-13 did not influence blood pressure ( P = 0.59), dP/d tmax ( P = 0.26), or dP/d tmin ( P = 0.85) in dogs. However, heart rate dose-dependently increased > 70% ( P < 0.01), which was accompanied by a significant increase in coronary blood flow ( P < 0.05) and reductions in left ventricular end-diastolic volume and stroke volume ( P < 0.001). In contrast, (pyr)apelin-13 did not significantly affect hemodynamics, coronary blood flow, or indexes of contractile function in pigs. Furthermore, swine studies found no effect of intracoronary (pyr)apelin-13 administration on coronary blood flow ( P = 0.83) or vasorelaxation in isolated, endothelium-intact ( P = 0.89) or denuded ( P = 0.38) coronary artery rings. Examination of all data across (pyr)apelin-13 concentrations revealed an exponential increase in cardiac output as peripheral resistance decreased across pigs and dogs ( P < 0.001; R2 = 0.78). Assessment of the Frank-Starling relationship demonstrated a significant linear relationship between left ventricular end-diastolic volume and stroke volume across species ( P < 0.001; R2 = 0.70). Taken together, these findings demonstrate that (pyr)apelin-13 does not directly influence myocardial contractility or coronary blood flow in either dogs or pigs. NEW & NOTEWORTHY Our findings provide much needed insight regarding the pharmacological cardiac and coronary effects of (pyr)apelin-13 in larger animal preparations. In particular, data highlight distinct hemodynamic responses of apelin across species, which are independent of any direct effect on myocardial contractility or perfusion.