AI Article Synopsis
- The study examines how vascular smooth muscle cells contribute to neointima formation after vascular injury, focusing on the role of specific protein tyrosine phosphatases (PTPs) like PTP-1B and SHP-2.* -
- Researchers hypothesized that injury to rat carotid arteries increases PTP expression and that certain growth factors, particularly PDGF and bFGF, elevate these PTP levels in cultured rat smooth muscle cells.* -
- Results confirmed that balloon catheter-induced vascular injury enhances PTP protein levels in a specific way, while only PDGF and bFGF (but not other factors) effectively increased PTP levels in vitro.*
Article Abstract
Migration and proliferation of vascular smooth muscle cells are key events in injury-induced neointima formation. Several growth factors and ANG 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 (PTP)-1B (PTP-1B). In the present study, we tested the following hypotheses: 1) rat carotid artery injury induces the expression of PTP-1B, Src homology-2 domain phosphatase (SHP-2), and PTP-proline, glutamate, serine, and threonine sequence (PEST) protein; and 2) polypeptide growth factors as well as ANG 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 ANG II, increases PTP-1B, SHP-2, and PTP-PEST protein levels. These results suggest that increased PDGF and bFGF levels, occurring after vascular injury, may induce expression of several PTPs.
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| http://dx.doi.org/10.1152/ajpheart.00520.2004 | DOI Listing |
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