Medical Journals

Mechanism of Isoproterenol-induced Rgs2 Up-regulation in Astrocytes.

Authors:
  • Kim Sung Dae
  • Lee Whi Min
  • Suk Kyoungho
  • Park Seung Chun
  • Kim Sang Keun
  • Cho Jae Youl
  • Rhee Man Hee

From: Laboratory of Physiology and Signaling, College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, Republic of Korea.

Biochemical and biophysical research communications

  • Publish Date: Oct 2006
  • ISSN: 0006-291X
  • Volume: 349
  • Issue: 1
  • Pages: 408-15
  • Medium: Print
  • Language: English
  • Citation (JAMA): Kim Sung Dae, Lee Whi Min, Suk Kyoungho, et al. Mechanism of Isoproterenol-induced Rgs2 Up-regulation in Astrocytes.. Biochem. Biophys. Res. Commun. Oct 2006;349:408-15

Abstract

Regulators of G protein signaling (RGSs) are inducibly expressed in response to various stimuli and the up-regulation of RGSs leads to significant decreases in GPCR responsiveness. Isoproterenol, an adrenergic receptor agonist, stimulated RGS2 mRNA in C6 rat astrocytoma cells. The up-regulation of RGS2 mRNA was abrogated by genistein, a protein tyrosine kinase inhibitor (PTK), and by broad-spectrum protein kinase C (PKC) inhibitors (staurosporine and GF109203X). alpha-Adrenergic antagonist (prazocin), beta-adrenergic antagonist (prazocin), and pertussis toxin only partially blocked the RGS2 up-regulation, suggesting that the RGS2 up-regulation is concomitantly mediated by Galphai, Galphas, and Galphaq. It is interesting to note that SB203580, a potent p38 mitogen-activated protein kinase (MAPK) inhibitor, completely inhibited the isoproterenol-mediated RGS2 expression. In addition, isoproterenol also markedly stimulated RGS2 mRNA in rat primary astrocytes, which were sensitive to SB203580 and staurosporine. Therefore, our data suggest that adrenergic receptor-mediated signaling (induced by isoproterenol) may be involved in the regulation of RGS2 expression in astrocytes via activating PTK, PKC, and p38 MAPK.

Mesh Headings (Keywords): Animals, Astrocytes, Cell Line, Tumor, Dose-Response Relationship, Drug, Enzyme Inhibitors, Gene Expression Regulation, Neoplastic, Genistein, Isoproterenol, MAP Kinase Signaling System, Protein Kinase C, RGS Proteins, Rats, Up-Regulation, p38 Mitogen-Activated Protein Kinases


Check for Full Text / PubMed Unique Identifier (PMID): 16934753


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