Open AccessGPR39 Is Coupled to TMEM16A in Intestinal Fibroblast-Like Cells
Author(s) -
Fanning Zeng,
Nicholas Wind,
Conor McClenaghan,
J. Martin Verkuyl,
Robert P. Watson,
Mark S. Nash
Publication year - 2012
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0047686
Subject(s) - motility , microbiology and biotechnology , fibroblast , regulator , population , small intestine , biology , chemistry , cell culture , endocrinology , biochemistry , medicine , genetics , gene , environmental health
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.