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Steroid-Mediated Regulation of the Epithelial Sodium Channel Subunits in Mammary Epithelial Cells

Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire 03756

Address all correspondence and requests for reprints to: Anikó Náray-Fejes-Tóth, Department of Physiology, Dartmouth Medical School, Borwell Building 744W, 1 Medical Center Drive, Lebanon, New Hampshire 03756. E-mail: aniko.fejes-toth{at}dartmouth.edu.

The epithelial sodium channel (ENaC) is a key mediator of sodium transport in epithelia; however, little is known about ENaC expression in mammary epithelia. Using real-time PCR, we demonstrated the expression of the ENaC subunit mRNAs in mouse and human mammary cell lines and in vivo mouse mammary tissue. We determined the effects of glucocorticoids, progesterone, and prolactin on ENaC expression in four mammary cell lines. Dexamethasone induced all detectable ENaC subunits in noncancerous cell lines, HC11 and MCF10A. Interestingly, in cancerous cell lines (T-47D and MCF-7), both ß- and - but not ENaC mRNAs were induced by dexamethasone. Progesterone induced ENaC mRNA only in T-47D cells, and prolactin had no effects. ENaC was rapidly induced by steroids, whereas induction of - and ßENaC was slower; moreover, the induction of the ß-subunit required de novo protein synthesis. Dexamethasone treatment did not affect ENaC mRNA stability. Western blot analysis revealed immunoreactive bands corresponding to different forms of -, ß-, and ENaC; dexamethasone significantly increased the intensity of ENaC (85 kDa) and ßENaC (90 kDa). We also showed an in vivo reduction in ENaC levels in the mammary tissue of lactating mice as compared with controls, whereas ß- and ENaC mRNA levels were significantly increased. Furthermore, dexamethasone in vivo significantly increased -, ß-, and ENaC mRNA expression. Our data indicate that both mouse and human mammary cells express all ENaC subunits, and they are regulated by steroid hormones in a temporal and cell-specific manner both in culture and in vivo.