scholarly journals Resveratrol ameliorates polycystic ovary syndrome via transzonal projections within oocyte-granulosa cell communication

Theranostics ◽  
2022 ◽  
Vol 12 (2) ◽  
pp. 782-795
Author(s):  
Mingyue Chen ◽  
Chengyong He ◽  
Kongyang Zhu ◽  
Zihan Chen ◽  
Zixiao Meng ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Granulosa Cell ◽  
Polycystic Ovary ◽  
Cell Communication ◽  
Ovary Syndrome

scholarly journals The effect of estradiol on granulosa cell responses to FSH in women with polycystic ovary syndrome

2017 ◽  
Vol 15 (1) ◽  
Author(s):  
Michael V. Homer ◽  
Marcus A. Rosencrantz ◽  
Rana F. Shayya ◽  
R. Jeffrey Chang
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Granulosa Cell ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Cell Responses

Altered miR-186 and miR-135a contribute to granulosa cell dysfunction by targeting ESR2: A possible role in polycystic ovary syndrome

2019 ◽  
Vol 494 ◽  
pp. 110478 ◽  
Author(s):  
Yuxia Song ◽  
Guo Yu ◽  
Yungai Xiang ◽  
Yan Li ◽  
Lijing Wan ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Granulosa Cell ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Cell Dysfunction

scholarly journals Reproductive and metabolic determinants of granulosa cell dysfunction in normal-weight women with polycystic ovary syndrome

2018 ◽  
Vol 109 (3) ◽  
pp. 508-515 ◽  
Author(s):  
Annie A. Guedikian ◽  
Alexandria Y. Lee ◽  
Tristan R. Grogan ◽  
David H. Abbott ◽  
Karla Largaespada ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Granulosa Cell ◽  
Polycystic Ovary ◽  
Normal Weight ◽  
Ovary Syndrome ◽  
Cell Dysfunction

scholarly journals microRNA-194 is increased in polycystic ovary syndrome granulosa cell and induce KGN cells apoptosis by direct targeting heparin-binding EGF-like growth factor

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Yi-xuan Wu ◽  
Yan-shan Lin ◽  
Si-chen Li ◽  
Xi Yao ◽  
Mingwei Cheng ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Polycystic Ovary Syndrome ◽  
Granulosa Cell ◽  
Polycystic Ovary ◽  
Luciferase Reporter ◽  
Heparin Binding ◽  
Ovary Syndrome ◽  
Proliferation And Apoptosis ◽  
Apoptotic Effects

Abstract Background Polycystic ovary syndrome (PCOS) is an endocrine-related follicular developmental disorder that affects 50 %-70 % of reproductive-aged women diagnosed with ovulation-related infertility. Abnormal proliferation and apoptosis of granulosa cells (GCs) are thought to be the critical factors leading to abnormal maturation of follicles. It has been shown that microRNAs (miRNAs) exert a significant influence in the pathogenesis of PCOS; however, the relationship between miRNA, PCOS, and GC apoptosis is not entirely understood. Methods To clarify the effect of miR-194 in PCOS, CCK-8, Ki67 staining, AO/EB, and flow cytometry assays were used to assess cell growth, proliferation, and apoptosis in KGN cells, which were artificially stimulated to overexpress miR-194. Luciferase reporter assays and rescue experiments were used to elucidate the mechanism underlying miR-194 in PCOS. Results miR-194 expression was significantly up-regulated in rat models of PCOS and the ovarian GCs of PCOS patients. miR-194 suppression promoted KGN cell growth and proliferation. miR-194 overexpression also induced cell apoptosis, while miR-194 downregulation had an opposite effect. Furthermore, up-regulating heparin-binding EGF-like growth factor (HB-EGF) expression rescued the pro-apoptotic effects of miR-194 upregulation on KGN cells. Conclusions miR-194 is increased in PCOS granulosa cell and may function as a novel biomarker and therapeutic target for KGN cells via HB-EGF regulation.

scholarly journals The Effect of Androgen Blockade on Granulosa Cell Estradiol Production after Follicle-Stimulating Hormone Stimulation in Women with Polycystic Ovary Syndrome

2006 ◽  
Vol 91 (9) ◽  
pp. 3503-3506 ◽  
Author(s):  
Rinku V. Mehta ◽  
Pamela J. Malcom ◽  
R. Jeffrey Chang
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Granulosa Cell ◽  
Polycystic Ovary ◽  
Follicular Development ◽  
Dehydroepiandrosterone Sulfate ◽  
Ovary Syndrome ◽  
Before And After ◽  
Normal Women ◽  
17 Hydroxyprogesterone

Abstract Context: Previously, we have shown that women with polycystic ovary syndrome (PCOS) exhibit an exaggerated serum estradiol (E2) response to recombinant human FSH (rhFSH) (150 IU) compared with similarly treated normal women. This enhanced granulosa cell responsiveness is consistent with excessive follicular development after gonadotropin therapy and the corresponding risk of ovarian hyperstimulation syndrome. In vitro studies have shown that granulosa cells treated with androgens display greater FSH-induced E2 production than untreated cells, suggesting a role for androgens in granulosa cell responsiveness. Main Objective: This study was conducted to determine whether blockade of androgen action in PCOS women by administration of the antiandrogen flutamide would alter E2 responses to rhFSH. Design: We conducted a prospective cohort study. Subjects and Setting: We studied 11 women with PCOS at an institutional general clinical research center. Intervention: On study d 1, each subject received 150 IU rhFSH iv. Frequent blood samples were obtained over 24 h. After completion of rhFSH stimulation, each subject was treated with flutamide, 125 mg, twice daily, for 6 wk. Thereafter, the rhFSH stimulation test was repeated. Main Outcome Measures: Baseline and stimulated E2 levels before and after treatment were assayed. Results: Mean baseline and maximally stimulated E2, integrated E2 response, and fold change in E2 were not different before and after treatment. Levels of testosterone, androstenedione, progesterone, 17-hydroxyprogesterone, estrone, and SHBG before and after treatment were unchanged. Baseline dehydroepiandrosterone sulfate levels declined significantly after flutamide therapy. Conclusion: These findings indicate that in women with PCOS, the E2 hyperresponsiveness to FSH may not be attributable to increased circulating androgens.

Sign in / Sign up

Export Citation Format

Share Document