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7 Integrin Expression in Vascular Smooth Muscle by Injury Induced Atherosclerosis
1 Cardiovascular Research Institute, Division of Vascular Biology, Texas A&M University Systems, Health Science Center, College Station, TX, USA
2 Center for Evironmental and Rural Health, Texas A&M University Systems, College Station, TX, USA; Department of Biochemistry and Molecular Biology, University of Louisville, Louisville, KY, USA
3 Center for Evironmental and Rural Health, Texas A&M University Systems, College Station, TX, USA; Department of Environmental Health Sciences, University of chicago, Ann Arbor, MI, USA
4 Department of Cell and Structural Biology, University of Illnois, Urbana, IL, USA
5 Cardiovascular Research Institute, Division of Vascular Biology, Texas A&M University Systems, Health Science Center, College Station, TX, USA; Center for Evironmental and Rural Health, Texas A&M University Systems, College Station, TX, USA; Department of Biochemistry and Molecular Biology, University of Louisville, Louisville, KY, USA
6 Cardiovascular Research Institute, Division of Vascular Biology, Texas A&M University Systems, Health Science Center, College Station, TX, USA; Center for Evironmental and Rural Health, Texas A&M University Systems, College Station, TX, USA
* To whom correspondence should be addressed. E-mail: emilyw{at}tamu.edu.
Objective: Injury of vascular smooth muscle cells (VSMC) by allylamine (AAM) leads to phenotypic changes associated with atherogenic progression, including increased proliferation, migration, and alterations in cell adhesion. In the present study, the relationship between AAM-induced vascular injury and expression of 
7 integrin subunit was investigated.
Methods: 7 mRNA and protein expression were examined using real-time RT-PCR, fluorescence-activated cell sorting analysis (FACS), immunohistochemistry, and immunoblotting.
Results: In cultured VSMC from aortas of AAM treated rats (70mg/kg; 20 days), 7 mRNA expression was increased greater than 2-fold, compared to control cells. No change was seen in 
1 integrin expression. FACS analysis revealed increased cell surface expression of 7 protein (25±9 %; *p<0.05). AAM treatment of naive VSMC enhanced 7 mRNA expression (2.4±0.7 fold, *p<0.05). The increased 7 mRNA expression was attenuated by semicarbazide, an amine oxidase inhibitor, and pyrrolidine dithiocarbamate (PDTC), an antioxidant, confirming a role for oxidative stress in modulating 7 expression. In vivo 7 mRNA and protein expression were enhanced in the aortas of AAM-treated rats. In addition, increased 7 integrin expression facilitated AAM VSMC adhesion to laminin more efficiently, compared to control (51±2%, *p<0.05).
Conclusion: Chemical injury induced by AAM enhances significantly 7 integrin expression in VSMC. These findings implicate, for the first time, the expression of 7 integrin during the response of VSMC to vascular injury.
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