NDLI: Metformin inhibits StAR expression in human endometriotic stromal cells via AMPK-mediated disruption of CREB-CRTC2 complex formation.

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Metformin inhibits StAR expression in human endometriotic stromal cells via AMPK-mediated disruption of CREB-CRTC2 complex formation.

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Metformin inhibits StAR expression in human endometriotic stromal cells via AMPK-mediated disruption of CREB-CRTC2 complex formation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhou, Yan Peng, Chao Zhou, Ying-Fang Xu, Jia-Ning Zeng, Cheng Xue, Qing
Description	Author Affiliation: Xu JN ( Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing 100034, People's Republic of China.)
Abstract	CONTEXT: Endometriosis is an estrogen-dependent disease affecting reproductive women. Metformin could have a therapeutic effect on endometriosis through regulation of local estrogen production. OBJECTS: The aim of this study was to investigate the molecular and cellular mechanism by which metformin regulates StAR expression in human endometriotic stromal cells (ESCs). METHODS: ESCs derived from ovarian endometriomas were cultured with metformin and prostaglandin E2 (PGE2). StAR mRNA was measured by quantitative PCR; pregnenolone, progesterone, and estrogen production were measured by ELISA kits; steroidogenic acute regulatory protein (StAR), AMP-activated protein kinase, cAMP response element binding protein (CREB), and CREB-regulated transcription coactivator 2 (CRTC2) protein expression were measured by Western blot assay; and CRTC2 translocation and its association with CREB were assessed by coimmunoprecipitation assay and CRTC2-CREB complex binding by a chromatin immunoprecipitation assay. RESULTS: 1) StAR mRNA levels in ESCs are 264 times higher than those in endometrial cells. 2) Metformin downregulates the StAR mRNA expression (maximum 31.7%) stimulated by PGE2 (2.4-fold) in ESCs. 3) PGE2 induces CRTC2 translocation and enhances its association with CREB to form a transcription complex that binds to the StAR promoter region. 4) Metformin prevents the nuclear translocation of CRTC2 by increasing AMP-activated protein kinase phosphorylation. This inhibits transcription of StAR by disrupting formation of the CREB-CRTC2 complex, involved in activation of the StAR promoter cAMP response element. CONCLUSIONS: We have demonstrated a detailed mechanistic analysis of StAR expression regulated by metformin in ESCs. Our data highlight a role for CRTC2 in the mechanism by which metformin inhibits StAR expression.
ISSN	0021972X
e-ISSN	19457197
Journal	The Journal of Clinical Endocrinology & Metabolism
Issue Number	8
Volume Number	99
Language	English
Publisher	Oxford University Press
Publisher Date	2014-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Amp-activated Protein Kinases Metabolism Endometrium Drug Effects Metformin Pharmacology Phosphoproteins Genetics Stromal Cells Cells, Cultured Cyclic Amp Response Element-binding Protein Down-regulation Phosphorylation Protein Binding Signal Transduction Transcription Factors Research Support, Non-u.s. Gov't Discipline Endocrinology Discipline Metabolism
Content Type	Text
Resource Type	Article
Subject	Biochemistry (medical) Endocrinology, Diabetes and Metabolism Clinical Biochemistry Biochemistry Endocrinology

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