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Departments of Pediatrics (X.H., Y.T., M.L., S.K.De., S.K.Da.), Cancer Biology (X.H., Y.T., M.L., S.K.Da.), Cell & Developmental Biology (S.K.De.) and Pharmacology (S.K.De.), Vanderbilt University Medical Center, Nashville, Tennessee 37232; and Laboratory Animal Center (Y.T.), Chongqing University of Medical Sciences, Chongqing 400016, People’s Republic of China
Address all correspondence and requests for reprints to: Dr. Sanjoy Das, Division of Reproductive and Developmental Biology, Department of Pediatrics, D-4105 Medical Center North, Vanderbilt University Medical Center, 1161 21st Avenue South, Nashville, Tennessee 37232-2678. E-mail: sanjoy.das{at}vanderbilt.edu.
Major biological effects of estrogen in the uterus are thought to be primarily mediated by nuclear estrogen receptors, ER
and ERß. 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 ß-catenin. We observed that estrogen treatment prompts nuclear localization of active ß-catenin in the uterine epithelium. We also found that adenovirus mediated in vivo delivery of SFRP-2, a Wnt antagonist, down-regulates estrogen-dependent ß-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/ß-catenin signaling in an ER-independent manner to regulate the late uterine growth response that is ER dependent.
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