Table of Contents
Journal of Signal Transduction
Volume 2012, Article ID 192142, 15 pages
Research Article

Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl Secretion in Mammary Epithelia

1Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL 60612, USA
2Department of Physiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand
3Department of Biological Sciences, Benedictine University, Lisle, IL 60532, USA
4Obstetrics, Gynecology and Reproductive Biology, Michigan State University, Grand Rapids, MI 49503, USA

Received 16 April 2012; Accepted 22 May 2012

Academic Editor: Jesus Garcia

Copyright © 2012 Utchariya Anantamongkol et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mammary gland ion transport is essential for lactation and is regulated by prolactin and glucocorticoids. This study delineates the roles of prolactin receptors (PRLR) and long-term prolactin and dexamethasone (P-D)-mediation of [Ca2+]i and Cl transport in HC-11 cells. P-D (24 h) suppressed ATP-induced [Ca2+]i. This may be due to decreased Ca2+ entry since P-D decreased transient receptor potential channel 3 (TRPC3) but not secretory pathway Ca2+-ATPase 2 (SPCA2) mRNA. ATP increased Cl transport, measured by iodide (I) efflux, in control and P-D-treated cells. P-D enhanced I efflux response to cAMP secretagogues without altering Cl channels or NKCC cotransporter expression. HC-11 cells contain only the long form of PRLR (PRLR-L). Since the short isoform, PRLR-S, is mammopoietic, we determined if transfecting PRLR-S (rs) altered PRLR-L-mediated Ca2+ and Cl transport. Untreated rs cells showed an attenuated [Ca2+]i response to ATP with no further response to P-D, in contrast to vector-transfected (vtc) controls. P-D inhibited TRPC3 in rs and vtc cells but increased SPCA2 only in rs cells. As in wild-type, cAMP-stimulated Cl transport, in P-D-treated vtc and rs cells. In summary, 24 h P-D acts via PRLR-L to attenuate ATP-induced [Ca2+]i and increase cAMP-activated Cl transport. PRLR-S fine-tunes these responses underscoring its mammopoietic action.