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Role of Regulators of G-Protein Signaling 4 in $Ca^{2+}$ Signaling in Mouse Pancreatic Acinar Cells

  • Park, Soon-Hong (Department of Oral Biology, Yonsei University College of Dentistry) ;
  • Lee, Syng-Ill (Department of Oral Biology, Yonsei University College of Dentistry) ;
  • Shin, Dong-Min (Department of Oral Biology, Yonsei University College of Dentistry)
  • Received : 2011.10.17
  • Accepted : 2011.11.08
  • Published : 2011.12.30

Abstract

Regulators of G-protein signaling (RGS) proteins are regulators of $Ca^{2+}$ 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 $Ca^{2+}$ 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.

Keywords

References

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