Open AccessA candidate pathogenic gene, zinc finger gene 217 ( ZNF 217 ), may contribute to polycystic ovary syndrome through prostaglandin E2
Author(s) -
Zhai Junyu,
Li Shang,
Cheng Xiaoyue,
Chen ZiJiang,
Li Weiping,
Du Yanzhi
Publication year - 2020
Publication title -
acta obstetricia et gynecologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.401
H-Index - 102
eISSN - 1600-0412
pISSN - 0001-6349
DOI - 10.1111/aogs.13719
Subject(s) - polycystic ovary , medicine , zinc finger , gene , ovary , prostaglandin e2 , endocrinology , gynecology , genetics , biology , insulin resistance , insulin , transcription factor
Polycystic ovary syndrome is a complex endocrine condition with chronic inflammation. Prostaglandin E2 ( PGE 2) is a proinflammatory factor with an increased expression in the serum of women with polycystic ovary syndrome. Zinc finger gene 217 ( ZNF 217 ) is known as a candidate gene for polycystic ovary syndrome. We aimed to investigate the relation between ZNF 217 and PGE 2 in polycystic ovary syndrome. Material and methods We used a rat model of dehydroepiandrosterone‐induced polycystic ovary syndrome and human granulosa cells both of women with polycystic ovary syndrome and of women without the syndrome to measure ZNF 217 and other target gene expressions. In addition, we performed in vitro experiments with KGN human granulosa‐like tumor cells to verify the molecular mechanisms. Results ZNF 217 was decreased in the granulosa cells both of dehydroepiandrosterone‐treated rats and of women with polycystic ovary syndrome. Cyclooxygenase 2, a key enzyme of PGE 2 synthesis, was highly expressed in the granulosa cells of rats and women with the syndrome, and PGE 2 concentration was increased in the follicular fluid. Furthermore, decreased ZNF 217 expression was supposed to inhibit estradiol synthesis, which further promoted cyclooxygenase 2 and PGE 2 synthesis. At the same time, PGE 2 had an inhibitory effect on ZNF 217 expression in a dose‐dependent manner in KGN cells. Conclusions Decreased ZNF 217 expression in granulosa cells of women with polycystic ovary syndrome induced inflammation via PGE 2, and PGE 2 inhibited ZNF 217 expression to establish a feedback loop. This mechanism might account for the pathogenesis of polycystic ovary syndrome.