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7 Integrin-Mediated Adhesion and Expression by Platelet-Derived Growth Factor in Vascular Smooth Muscle Cells
1 Medical Physiology, Division of Vascular Biology, The Cardiovascular Research Institute, Texas A&M University System, HSC, College Station, TX, USA; Medical Pharmacology and Physiology, University of MIssouri, Columbia, MO, USA
2 Medical Physiology, Division of Vascular Biology, The Cardiovascular Research Institute, Texas A&M University System, HSC, College Station, TX, USA
3 Cell and Structural Biology, University of Illnois, Urbana, Urbana, IL, USA
4 Medical Physiology, Division of Vascular Biology, The Cardiovascular Research Institute, Texas A&M University System, HSC, College Station, TX, USA; Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA
5 Biochemistry and Molecular Biology, University of Louisville, Louisville, Louisville, KY, USA
* To whom correspondence should be addressed. E-mail: emilyw{at}tamu.edu.
We showed previously that the expression of 
7 integrin in aortic vascular smooth muscle cells (VSMC) is enhanced in a rat model of atherosclerosis. In the present study, we investigated the effects of platelet-derived growth factor (PDGF) on 7 integrin expression and VSMC adhesion and migration. Expression of the 7 integrin gene was determined by real-time RT-PCR while protein levels were determined by fluorescence-activated cell sorting analysis (FACS). PDGF increased 7 cell surface protein expression (12 and 24h: 3.3±0.8 and 3.6±0.4 fold, *p<0.05 vs. control) and mRNA levels (24h: 3.1 fold, *p<0.05 vs. control) in a time-dependent manner. Actinomycin D and cycloheximide attenuated PDGF-induced increases in 7 integrin, indicating the involvement of de novo mRNA and protein synthesis. Treatment with the MAP kinase inhibitors PD98059, SP600125, and SB203580, attenuated PDGF-induced increases in mRNA. In contrast, PD98059 and Sp600125, but not SB203580, attenuated PDGF-induced increases in cell surface protein levels. PDGF-treated VSMC adhered to laminin more efficiently (42±6% increase; **p<0.01), and this increase was partially inhibited by anti-7-integrin function blocking antibody. However, PDGF did not alter migration on laminin, and there was no effect of the anti-7 integrin function-blocking antibody on basal or PDGF-stimulated migration. Immunofluorescence imaging revealed an increase in 7 integrin distribution along the stress fibers. Together, these observations indicate that PDGF enhances 7 integrin expression in VSMC, and promotes 7 integrin mediated adhesion to laminin.
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