期刊
MOLECULAR ENDOCRINOLOGY
卷 18, 期 12, 页码 3035-3049出版社
OXFORD UNIV PRESS INC
DOI: 10.1210/me.2004-0259
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资金
- NICHD NIH HHS [HD12304, HD33994, P30 HD033994, U54 HD033994, HD37830, R01 HD037830, R37 HD012304] Funding Source: Medline
- NIEHS NIH HHS [R01 ES007814, ES07814] Funding Source: Medline
Major biological effects of estrogen in the uterus are thought to be primarily mediated by nuclear estrogen receptors, ERalpha and ERbeta. We show here that estrogen in an ER-independent manner rapidly up-regulates the expression of Wnt4 and Wnt5a of the Wnt family and frizzled-2 of the Wnt receptor family in the mouse uterus. One of the mechanisms by which Wnts mediate canonical signaling involves stabilization of intracellular beta-catenin. We observed that estrogen treatment prompts nuclear localization of active beta-catenin in the uterine epithelium. We also found that adenovirus mediated in vivo delivery of SFRP-2, a Wnt antagonist, downregulates estrogen-dependent beta-catenin activity without affecting some of the early effects ( water imbibition and angiogenic markers) and inhibits uterine epithelial cell growth, suggesting that canonical Wnt signaling is critical to estrogen-induced uterine growth. Our present results provide evidence for a novel role of estrogen that targets early Wnt/beta-catenin signaling in an ER-independent manner to regulate the late uterine growth response that is ER dependent.
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