Prolactin and dexamethasone regulate second messenger-stimulated cl(-) secretion in mammary epithelia.
Prolactin and dexamethasone regulate second messenger-stimulated cl(-) secretion in mammary epithelia.
复制标题
催乳素和地塞米松调节乳腺上皮细胞中第二信使刺激的 cl(-) 分泌。
DOI：
10.1155/2012/192142
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Rao,MrinaliniC
中科院分区：
文献类型：
--
作者：
Anantamongkol,Utchariya;Ao,Mei;SarathyNeeVenkatasubramanian,Jayashree;Devi,YSangeeta;Krishnamra,Nateetip;Rao,MrinaliniC
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+]iand 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+]iresponse 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+]iand increase cAMP‐activated Cl−transport. PRLR‐S fine‐tunes these responses underscoring its mammopoietic action.
