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1 Physiology, University of tennessee health science center, memphis, TN, USA
* To whom correspondence should be addressed. E-mail: ychang{at}physio1.utmem.edu.
Migration and proliferation of vascular smooth muscle cells are key events in injury-induced neointima formation. Several growth factors as well as angiotensin II are thought to be involved in neointima formation. A recent report indicated that vascular injury is associated with increased mRNA levels of protein tyrosine phosphatase 1B (PTP1B). In the current study we tested the following two hypotheses: 1) Rat carotid artery injury induces the expression of PTP1B, SHP2 and PTP-PEST protein, 2) Polypeptide growth factors as well as angiotensin II increase the levels of tyrosine phosphatases in cultured rat aortic smooth muscle cells. We found that vascular injury induced by balloon catheter increases the protein levels of aforementioned phosphatases and that these effects occur in a PTP-specific, as well as temporally and regionally specific manner. Moreover, treatment of cultured primary rat aortic smooth muscle cells with PDGF or bFGF, but not with IGF1, EGF or angiotensin II, increases PTP1B, SHP2 and PTP-PEST protein levels. These results suggest that increased PDGF and bFGF levels, occurring after vascular injury, may induce expression of several PTP.
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