Regulators of G-protein signaling (RGS) proteins are regulators of Ca 2+ signaling that accelerate the GTPase activity of the G-protein α-subunit. RGS1, RGS2, RGS4, and RGS16 are expressed in the pancreas, and RGS2 regulates G-protein coupled receptor (GPCR)-induced Ca 2+ oscillations. However, the role of RGS4 in Ca 2+ signaling in pancreatic acinar cells is unknown. In this study, we investigated the mechanism of GPCR-induced Ca 2+ 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 Ca 2+ oscillations. RGS4 -/- cells also showed increased expression of sarco/endoplasmic reticulum Ca 2+ ATPase type 2. However, there were no significant alterations, such as Ca 2+ 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 Ca 2+ signaling in mouse pancreatic acinar cells.
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