{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,18]],"date-time":"2025-10-18T10:01:47Z","timestamp":1760781707184},"reference-count":50,"publisher":"The Endocrine Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,8,1]]},"abstract":"<jats:p>Long-term estrogen actions are vital for driving cell growth, but more recent evidence suggests that estrogen mediates more rapid cellular effects. However, the function of estradiol-17\u03b2 (E2)-BSA in mouse embryonic stem cells has not been reported. Therefore, we examined the role of E2-BSA in mouse embryonic stem cell motility and its related signal pathways. E2-BSA (10\u22128m) significantly increased motility after 24 h incubation and increased filamentous (F)-actin expression; these effects were inhibited by the estrogen receptor antagonist ICI 182,780, indicating that E2-BSA bound membrane estrogen receptors and initiated a signal. E2-BSA increased c-Src and focal adhesion kinase (FAK) phosphorylation, which was attenuated by ICI 182,780. The E2-BSA-induced increase in epidermal growth factor receptor (EGFR) phosphorylation was inhibited by Src inhibitor PP2. As a downstream signal molecule, E2-BSA activated cdc42 and increased formation of a complex with the neural Wiskott-Aldrich syndrome protein (N-WASP)\/cdc42\/transducer of cdc42-dependent actin assembly-1 (TOCA-1), which was inhibited by FAK small interfering RNA (siRNA) and EGFR inhibitor AG 1478. In addition, E2-BSA increased profilin-1 expression and cofilin-1 phosphorylation, which was blocked by cdc42 siRNA. Subsequently, E2-BSA induced an increase in F-actin expression, and cell motility was inhibited by each signal pathway-related siRNA molecule or inhibitors but not by cofilin-1 siRNA. A combined treatment of cofilin-1 siRNA and E2-BSA increased F-actin expression and cell motility more than that of E2-BSA alone. These data demonstrate that E2-BSA stimulated motility by interacting with profilin-1\/cofilin-1 and F-actin through FAK- and c-Src\/EGFR transactivation-dependent N-WASP\/cdc42\/TOCA-1 complex.<\/jats:p>","DOI":"10.1210\/me.2012-1002","type":"journal-article","created":{"date-parts":[[2012,6,27]],"date-time":"2012-06-27T07:44:18Z","timestamp":1340783058000},"page":"1291-1303","source":"Crossref","is-referenced-by-count":11,"title":["Rapid Actions of Plasma Membrane Estrogen Receptors Regulate Motility of Mouse Embryonic Stem Cells through a Profilin-1\/Cofilin-1-Directed Kinase Signaling Pathway"],"prefix":"10.1210","volume":"26","author":[{"given":"Seung Pil","family":"Yun","sequence":"first","affiliation":[{"name":"Department of Veterinary Physiology (S.P.Y., J.M.R., M.O.K., J.H.P.), College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Korea;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jung Min","family":"Ryu","sequence":"additional","affiliation":[{"name":"Department of Veterinary Physiology (S.P.Y., J.M.R., M.O.K., J.H.P.), College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Korea;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mi Ok","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Veterinary Physiology (S.P.Y., J.M.R., M.O.K., J.H.P.), College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Korea;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jae Hong","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Veterinary Physiology (S.P.Y., J.M.R., M.O.K., J.H.P.), College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Korea;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ho Jae","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Veterinary Physiology (H.J.H.), College of 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