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Stimulation of G-protein coupled receptors in vascular smooth muscle cells induces tyrosine kinase dependent increases in calcium without tyrosine phosphorylation of phospholipase C γ-1

Authors
Journal
FEBS Letters
0014-5793
Publisher
Wiley Blackwell (John Wiley & Sons)
Publication Date
Volume
422
Issue
1
Identifiers
DOI: 10.1016/s0014-5793(97)01606-2
Keywords
  • Angiotensin-Ii
  • Cellular Ca2+
  • Endothelin
  • G-Protein Coupled Receptor
  • Fura-2
  • Genistein
  • Phospholipase C
  • Platelet Derived Growth Factor
  • Protein Tyrosine Phosphorylation
  • Serotonin
  • Vascular Smooth Muscle Cell
  • Vasopressin
Disciplines
  • Biology

Abstract

Abstract It is often believed that increases in intracellular Ca 2+ ([Ca 2+] i) resulting from stimulation of G-protein coupled receptors in vascular smooth muscle cells (VSMC) require activation of the β1 isoform of phospholipase C (PLC). However, recent studies showed that rat aortic VSMC do not express PLC β-1 and that stimulation with angiotensin-II induces tyrosine kinase dependent increases in [Ca 2+] i and tyrosine phosphorylation of PLC γ-1. Whether this pathway is activated by other vasoactive agents that stimulate G-protein coupled receptors is unknown. Here, we show that A10 VSMC express PLC β-2, PLC β-3, PLC δ-1, and PLC γ-1. The cells also expressed Gα q/11. However, neither PLC β-1 nor PLC β-4 was detected. Stimulation with angiotensin-II, vasopressin, serotonin, or endothelin induced tyrosine kinase dependent increases in [Ca 2+] i. However, tyrosine phosphorylation of PLC γ-1 did not occur. In contrast, stimulation with platelet derived growth factor increased [Ca 2+] i and tyrosine phosphorylation of PLC γ-1. The results show that tyrosine phosphorylation of PLC γ-1 is not required for tyrosine kinase dependent increases in [Ca 2+] i resulting from stimulation of diverse G-protein coupled receptors in VSMC.

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