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Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl(−) Secretion in Mammary Epithelia
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 A...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410352/ https://www.ncbi.nlm.nih.gov/pubmed/22888420 http://dx.doi.org/10.1155/2012/192142 |
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author | Anantamongkol, Utchariya Ao, Mei Sarathy nee Venkatasubramanian, Jayashree Devi, Y. Sangeeta Krishnamra, Nateetip Rao, Mrinalini C. |
author_facet | Anantamongkol, Utchariya Ao, Mei Sarathy nee Venkatasubramanian, Jayashree Devi, Y. Sangeeta Krishnamra, Nateetip Rao, Mrinalini C. |
author_sort | Anantamongkol, Utchariya |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3410352 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-34103522012-08-10 Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl(−) Secretion in Mammary Epithelia Anantamongkol, Utchariya Ao, Mei Sarathy nee Venkatasubramanian, Jayashree Devi, Y. Sangeeta Krishnamra, Nateetip Rao, Mrinalini C. J Signal Transduct Research Article 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. Hindawi Publishing Corporation 2012 2012-07-25 /pmc/articles/PMC3410352/ /pubmed/22888420 http://dx.doi.org/10.1155/2012/192142 Text en Copyright © 2012 Utchariya Anantamongkol et al. https://creativecommons.org/licenses/by/3.0/ 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. |
spellingShingle | Research Article Anantamongkol, Utchariya Ao, Mei Sarathy nee Venkatasubramanian, Jayashree Devi, Y. Sangeeta Krishnamra, Nateetip Rao, Mrinalini C. Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl(−) Secretion in Mammary Epithelia |
title | Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl(−) Secretion in Mammary Epithelia |
title_full | Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl(−) Secretion in Mammary Epithelia |
title_fullStr | Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl(−) Secretion in Mammary Epithelia |
title_full_unstemmed | Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl(−) Secretion in Mammary Epithelia |
title_short | Prolactin and Dexamethasone Regulate Second Messenger-Stimulated Cl(−) Secretion in Mammary Epithelia |
title_sort | prolactin and dexamethasone regulate second messenger-stimulated cl(−) secretion in mammary epithelia |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410352/ https://www.ncbi.nlm.nih.gov/pubmed/22888420 http://dx.doi.org/10.1155/2012/192142 |
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