Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl− Secretion inMammary Epithelia
journal contributionposted on 2013-11-15, 00:00 authored by Utchariya Anantamongkol, Mei Ao, Y. Sangeeta Devi, Nateetip Krishnamra, Mrinalini C. Rao, Jayashree Sarathy nee Venkatasubramanian
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 [Ca(2+)](i) and Cl(-) transport in HC-11 cells. P-D (24 h) suppressed ATP-induced [Ca(2+)](i). This may be due to decreased Ca(2+) entry since P-D decreased transient receptor potential channel 3 (TRPC3) but not secretory pathway Ca(2+)-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 Ca(2+) and Cl(-) transport. Untreated rs cells showed an attenuated [Ca(2+)](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 [Ca(2+)](i) and increase cAMP-activated Cl(-) transport. PRLR-S fine-tunes these responses underscoring its mammopoietic action.
National Institute of Diabetes and Digestive and Kidney Diseases (1 P01 DK067887 Project 3) (to M. C. Rao and R. V. Benya), grants from the National Institutes of Health HD11119 and HD 12356 (P. I.: Professor Geula Gibori; Trainee: Y. S. Devi).
Publisher StatementCopyright © 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. The original version is available through Hindawi Publishing Corporation at DOI: 10.1155/2012/192142
PublisherHindawi Publishing Corporation