Angiotensin II induces 3CH134, a protein-tyrosine phosphatase, in vascular smooth muscle cells.
Angiotensin II is a potent growth factor for vascular smooth muscle cells and shares many signal transduction mechanisms with mitogens, including stimulation of mitogen-activated protein (MAP) kinases and protein tyrosine phosphorylation. Regulation of tyrosine phosphorylation involves both protein-tyrosine kinases and protein-tyrosine phosphatases (PTPases). To investigate the role of PTPases in angiotensin II-mediated events, we studied the expression of a transcriptionally regulated PTPase, 3CH134, which has selective activity toward MAP kinase. Angiotensin II rapidly induced 3CH134 mRNA (30 min maximum) in a concentration-dependent manner (100 nM maximum). Platelet-derived growth factor, alpha-thrombin, hydrogen peroxide, phorbol 12-myristate 13-acetate, and ionomycin also induced 3CH134 but to levels lower than angiotensin II. Induction of 3CH134 by angiotensin II was partially inhibited after down-regulating protein kinase C but was fully inhibited after chelating intracellular Ca2+. Treatment with both phorbol 12-myristate 13-acetate and ionomycin induced 3CH134 mRNA to levels seen with angiotensin II, indicating that Ca2+ mobilization and protein kinase C activation can act synergistically to induce 3CH134. Angiotensin II stimulated 3CH134 protein synthesis after 1 h as measured by immunoprecipitation of 3CH134 from [35S]methionine-labeled cells using affinity-purified antibodies. These results establish 3CH134 as a dynamically regulated, immediate early gene in vascular smooth muscle cells and suggest a role for PTPases in regulating angiotensin II-stimulated events mediated by MAP kinases and tyrosine kinases.[1]References
- Angiotensin II induces 3CH134, a protein-tyrosine phosphatase, in vascular smooth muscle cells. Duff, J.L., Marrero, M.B., Paxton, W.G., Charles, C.H., Lau, L.F., Bernstein, K.E., Berk, B.C. J. Biol. Chem. (1993) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
