Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl− Secretion in Mammary Epithelia. (30th May 2012)

• Record Type: Journal Article
• Authors: Anantamongkol, Utchariya; Ao, Mei; Sarathy nee Venkatasubramanian, Jayashree; Devi, Y. Sangeeta; Krishnamra, Nateetip; Rao, Mrinalini C.
• Other Names: Garcia Jesus Academic Editor.
• Is Part Of: Journal of signal transduction. Volume 2012(2012)
• Publication Date: 2012-05-30
• Subjects: Cellular signal transduction -- Periodicals; Signal Transduction; Cellular signal transduction; Periodical; Periodicals; Electronic journals; 616.0277
• DOI: 10.1155/2012/192142
• Languages: English
• ISSNs: 2090-1739

Abstract

Abstract : 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.