Role of Regulators of G-Protein Signaling 4 in Ca2+ Signaling in Mouse Pancreatic Acinar Cells

被引：4

作者：

Park, Soonhong ^{[1
]}

Lee, Syng-Ill ^{[1
]}

Shin, Dong Min ^{[1
]}

机构：

[1] Yonsei Univ, Dept Oral Biol, Coll Dent, Seoul 120752, South Korea

来源：

KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY | 2011年 / 15卷 / 06期

基金：

新加坡国家研究基金会;

关键词：

RGS4; Ca2+ signaling; Pancreatic acinar cells; GTPASE-ACTIVATING PROTEINS; ALPHA-FACTOR PHEROMONES; RGS PROTEINS; INOSITOL TRISPHOSPHATE; A-FACTOR; OSCILLATIONS; RELEASE; SPECIFICITY; DYNAMICS; CHANNELS;

D O I：

10.4196/kjpp.2011.15.6.383

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Regulators of G-protein signaling (RGS) proteins are regulators of Ca2+ signaling that accelerate the GTPase activity of the G-protein alpha -subunit. RGS1, RGS2, RGS4, and RGS16 are expressed in the pancreas, and RGS2 regulates G-protein coupled receptor (GPCR)-induced Ca2+ oscillations. However, the role of RGS4 in Ca2+ signaling in pancreatic acinar cells is unknown. In this study, we investigated the mechanism of GPCR-induced Ca2+ signaling in pancreatic acinar cells derived from RGS4(-/-) mice. RGS4(-/-) acinar cells showed an enhanced stimulus intensity response to a muscarinic receptor agonist in pancreatic acinar cells. Moreover, deletion of RGS4 increased the frequency of Ca2+ oscillations. RGS4(-/-) cells also showed increased expression of sarco/endoplasmic reticulum Ca2+ ATPase type 2. However, there were no significant alterations, such as Ca2+ signaling in treated high dose of agonist and its related amylase secretion activity, in acinar cells from RGS4(-/-) mice. These results indicate that RGS4 protein regulates Ca2+ signaling in mouse pancreatic acinar cells.

引用

页码：383 / 388

页数：6

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