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Article: Testosterone Represses Estrogen Signaling by Upregulating miR-22: A Mechanism for Imbalanced Steroid Hormone Production in Preeclampsia

TitleTestosterone Represses Estrogen Signaling by Upregulating miR-22: A Mechanism for Imbalanced Steroid Hormone Production in Preeclampsia
Authors
Keywordsaromatase
estradiol
estrogen receptor alpha
pre-eclampsia
testosterone
Issue Date2017
Citation
Hypertension, 2017, v. 69, n. 4, p. 721-730 How to Cite?
AbstractPreeclampsia, a multisystem syndrome occurring during mid- to late gestation in humans, is a leading cause of maternal and perinatal morbidity and mortality. Patients usually present with high circulating testosterone and reduced estradiol production, but the mechanisms remain unclear. Revealing the mechanism that modulating the imbalance of testosterone and estradiol in preeclampsia is of great value in understanding the cause of the disease. The placenta is the predominant source of steroid hormone production during gestation, and we observed markedly increased 17β-HSD3 (17β-hydroxysteroid dehydrogenase 3) levels and downregulated aromatase expression, the key enzymes responsible for synthesis of testosterone and estradiol, respectively, in preeclamptic placentas compared with controls. Furthermore, we found a significant upregulation of microRNA (miR)-22 in preeclamptic placentas. In a trophoblast cell line, JEG-3 cells, testosterone repressed the expression of aromatase and estrogen receptor α and the production of estradiol while promoting miR-22 expression. miR-22 directly targeted and inhibited estrogen receptor α expression while indirectly decreasing aromatase expression and estradiol production by interfering with estrogen receptor α signaling. Furthermore, inhibition of miR-22 expression significantly reversed the inhibitory effect of testosterone on de novo estradiol synthesis in human trophoblastic cells. The findings reveal a mechanism underlying the balanced production of androgen and estrogen modulated by miR-22 in the human placenta and provide new insights into the pathogenesis of preeclampsia from the aspect of endocrine regulation.
Persistent Identifierhttp://hdl.handle.net/10722/355337
ISSN
2023 Impact Factor: 6.9
2023 SCImago Journal Rankings: 2.827

 

DC FieldValueLanguage
dc.contributor.authorShao, Xuan-
dc.contributor.authorLiu, Yanlei-
dc.contributor.authorLiu, Ming-
dc.contributor.authorWang, Yongqing-
dc.contributor.authorYan, Liying-
dc.contributor.authorWang, Hao-
dc.contributor.authorMa, Liyang-
dc.contributor.authorLi, Yu Xia-
dc.contributor.authorZhao, Yangyu-
dc.contributor.authorWang, Yan Ling-
dc.date.accessioned2025-04-03T02:00:08Z-
dc.date.available2025-04-03T02:00:08Z-
dc.date.issued2017-
dc.identifier.citationHypertension, 2017, v. 69, n. 4, p. 721-730-
dc.identifier.issn0194-911X-
dc.identifier.urihttp://hdl.handle.net/10722/355337-
dc.description.abstractPreeclampsia, a multisystem syndrome occurring during mid- to late gestation in humans, is a leading cause of maternal and perinatal morbidity and mortality. Patients usually present with high circulating testosterone and reduced estradiol production, but the mechanisms remain unclear. Revealing the mechanism that modulating the imbalance of testosterone and estradiol in preeclampsia is of great value in understanding the cause of the disease. The placenta is the predominant source of steroid hormone production during gestation, and we observed markedly increased 17β-HSD3 (17β-hydroxysteroid dehydrogenase 3) levels and downregulated aromatase expression, the key enzymes responsible for synthesis of testosterone and estradiol, respectively, in preeclamptic placentas compared with controls. Furthermore, we found a significant upregulation of microRNA (miR)-22 in preeclamptic placentas. In a trophoblast cell line, JEG-3 cells, testosterone repressed the expression of aromatase and estrogen receptor α and the production of estradiol while promoting miR-22 expression. miR-22 directly targeted and inhibited estrogen receptor α expression while indirectly decreasing aromatase expression and estradiol production by interfering with estrogen receptor α signaling. Furthermore, inhibition of miR-22 expression significantly reversed the inhibitory effect of testosterone on de novo estradiol synthesis in human trophoblastic cells. The findings reveal a mechanism underlying the balanced production of androgen and estrogen modulated by miR-22 in the human placenta and provide new insights into the pathogenesis of preeclampsia from the aspect of endocrine regulation.-
dc.languageeng-
dc.relation.ispartofHypertension-
dc.subjectaromatase-
dc.subjectestradiol-
dc.subjectestrogen receptor alpha-
dc.subjectpre-eclampsia-
dc.subjecttestosterone-
dc.titleTestosterone Represses Estrogen Signaling by Upregulating miR-22: A Mechanism for Imbalanced Steroid Hormone Production in Preeclampsia-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1161/HYPERTENSIONAHA.116.08468-
dc.identifier.pmid28193709-
dc.identifier.scopuseid_2-s2.0-85012909136-
dc.identifier.volume69-
dc.identifier.issue4-
dc.identifier.spage721-
dc.identifier.epage730-
dc.identifier.eissn1524-4563-

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