GPR39 is coupled to TMEM16A in intestinal fibroblast-like cells.

GPR39 is a GPCR implicated as a regulator of gastrointestinal motility, although the mechanism remains elusive. Here, we report that GPR39 is expressed by a specific cell population cultured from mouse small intestine muscle layers, which was subsequently identified as fibroblast-like cells (FLCs) t...

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Autores principales:	Fanning Zeng, Nicholas Wind, Conor McClenaghan, J Martin Verkuyl, Robert P Watson, Mark S Nash
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e1f8f916d1a84b629320d1992385407f
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spelling	oai:doaj.org-article:e1f8f916d1a84b629320d1992385407f2021-11-18T08:11:02ZGPR39 is coupled to TMEM16A in intestinal fibroblast-like cells.1932-620310.1371/journal.pone.0047686https://doaj.org/article/e1f8f916d1a84b629320d1992385407f2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23133519/?tool=EBIhttps://doaj.org/toc/1932-6203GPR39 is a GPCR implicated as a regulator of gastrointestinal motility, although the mechanism remains elusive. Here, we report that GPR39 is expressed by a specific cell population cultured from mouse small intestine muscle layers, which was subsequently identified as fibroblast-like cells (FLCs) that have recently been shown to modulate gut motility. Application of the GPR39 agonist, Zn(2+), induced large currents and membrane depolarization in FLCs cultured from wild-type mice, but not Gpr39(-/-) mice. This Zn(2+)-induced current could be suppressed by application of a TMEM16A antagonist, CaCC(inh)-A01, or by silencing Tmem16a expression. These data suggest that GPR39 might modulate gut motility via regulating TMEM16A function in FLCs.Fanning ZengNicholas WindConor McClenaghanJ Martin VerkuylRobert P WatsonMark S NashPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 10, p e47686 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Fanning Zeng Nicholas Wind Conor McClenaghan J Martin Verkuyl Robert P Watson Mark S Nash GPR39 is coupled to TMEM16A in intestinal fibroblast-like cells.
description	GPR39 is a GPCR implicated as a regulator of gastrointestinal motility, although the mechanism remains elusive. Here, we report that GPR39 is expressed by a specific cell population cultured from mouse small intestine muscle layers, which was subsequently identified as fibroblast-like cells (FLCs) that have recently been shown to modulate gut motility. Application of the GPR39 agonist, Zn(2+), induced large currents and membrane depolarization in FLCs cultured from wild-type mice, but not Gpr39(-/-) mice. This Zn(2+)-induced current could be suppressed by application of a TMEM16A antagonist, CaCC(inh)-A01, or by silencing Tmem16a expression. These data suggest that GPR39 might modulate gut motility via regulating TMEM16A function in FLCs.
format	article
author	Fanning Zeng Nicholas Wind Conor McClenaghan J Martin Verkuyl Robert P Watson Mark S Nash
author_facet	Fanning Zeng Nicholas Wind Conor McClenaghan J Martin Verkuyl Robert P Watson Mark S Nash
author_sort	Fanning Zeng
title	GPR39 is coupled to TMEM16A in intestinal fibroblast-like cells.
title_short	GPR39 is coupled to TMEM16A in intestinal fibroblast-like cells.
title_full	GPR39 is coupled to TMEM16A in intestinal fibroblast-like cells.
title_fullStr	GPR39 is coupled to TMEM16A in intestinal fibroblast-like cells.
title_full_unstemmed	GPR39 is coupled to TMEM16A in intestinal fibroblast-like cells.
title_sort	gpr39 is coupled to tmem16a in intestinal fibroblast-like cells.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/e1f8f916d1a84b629320d1992385407f
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_version_	1718422141749166080

GPR39 is coupled to TMEM16A in intestinal fibroblast-like cells.

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