First Author | Zeng F | Year | 2012 |
Journal | PLoS One | Volume | 7 |
Issue | 10 | Pages | e47686 |
PubMed ID | 23133519 | Mgi Jnum | J:192254 |
Mgi Id | MGI:5464224 | Doi | 10.1371/journal.pone.0047686 |
Citation | Zeng F, et al. (2012) GPR39 is coupled to TMEM16A in intestinal fibroblast-like cells. PLoS One 7(10):e47686 |
abstractText | 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. |