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
收藏
页码：383 / 388
页数：6
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