17β-Estradiol Induces Overproliferation in Adenomyotic Human Uterine Smooth Muscle Cells of the Junctional Zone Through Hyperactivation of the Estrogen Receptor-Enhanced RhoA/ROCK Signaling Pathway

Fu-Qing Sun, Fuqing Sun, Hua Duan, Sha Wang, Jin-Jiao Li
Reproductive sciences (Thousand Oaks, Calif.) · 2015 · vol. 22(11) , pp. 1436–1444 · doi:10.1177/1933719115584447 · PMID:25940707 · W2299216983
article OA: closed CC0 ⤵ 11 in-corpus citations
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-08 ⓘ

17β-estradiol induces overproliferation in adenomyotic uterine smooth muscle cells via estrogen receptor-enhanced RhoA/ROCK signaling, leading to cell cycle alterations.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

This study examined how 17β-estradiol (E2) affects proliferation-related signaling in human uterine smooth muscle cells (SMCs) from the junctional zone, comparing adenomyosis (ADS) cells with non-ADS cells. The authors found that E2 increased expression and hyperactivation of estrogen receptor (ER)-dependent RhoA and its downstream effectors ROCK1 and ROCK2, and this signaling was linked to overproliferation in ADS JZ SMCs, accompanied by downregulation of cyclin-dependent kinase inhibitors (p21Waf1/Cip1 and p27Kip1) and upregulation of multiple CDKs and cyclins. A key caveat is that the work is based on in vitro treatment of isolated cells rather than in vivo demonstration of causality. This paper is centrally about adenomyosis—specifically, it tests how ER-enhanced RhoA/ROCK signaling mediates E2-induced overproliferation in adenomyotic human uterine junctional zone smooth muscle cells.

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MeSH descriptors

Adenomyosis Cell Proliferation Estradiol Myocytes, Smooth Muscle Myometrium Receptors, Estrogen rhoA GTP-Binding Protein rho-Associated Kinases Signal Transduction Adenomyosis Adenomyosis Adenomyosis Cell Cycle Proteins Cell Cycle Proteins Cell Proliferation Cells, Cultured Estradiol Estrogen Antagonists Estrogen Antagonists Female

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