| Autor: |
Anantamongkol, Utchariya, Ao, Mei, Venkatasubramanian, Jayashree Sarathy nee, Devi, Y. Sangeeta, Krishnamra, Nateetip, Rao, Mrinalini C. |
| Zdroj: |
Journal of Signal Transduction; 2012, p1-15, 15p, 1 Chart, 7 Graphs |
| Abstrakt: |
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 vectortransfected (vtc) controls. P-D inhibited TRPC3 in rs and vtc cells but increased SPCA2 only in rs cells. As in wild-type, cAMPstimulated 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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