Objective-Intimal growth depends on smooth muscle cell (SMC) migration and proliferation and is regulated by thrombotic and inflammatory responses to vascular injury. Platelet-derived growth factor (PDGF)-BB and interleukin (IL)-1 have been shown to contribute to intimal hyperplasia and lesion progression in atherosclerosis. Mitogenic effects of IL-1 on SMCs have been reported and have been attributed to the expression of PDGF-A chain. In some, but not all, studies, IL-1 was found to cooperate with growth factors, including PDGF, in stimulating proliferation. The molecular basis for such cooperative effects is unknown and is the subject of the present study. Methods and Results-We demonstrate that in baboon aortic SMCs, IL-1 enhances the proliferation induced by PDGF-BB independently of PDGF-A signaling. IL-1 increases the phosphorylation of retinoblastoma protein, a pivotal step in the G 1 -to-S transition in the cell cycle. Analysis of expression levels of cyclins and cyclin-dependent kinase (CDK) inhibitors suggests that IL-1 stimulates CDKs by downregulating p21 and p27. Consistent with this hypothesis is the finding that CDK2 activity, induced by PDGF-BB, is enhanced 2.3Ϯ0.2-fold in the presence of IL-1. Key Words: smooth muscle Ⅲ platelet-derived growth factor Ⅲ interleukin-1 Ⅲ p21(WAF1/CIP1) Ⅲ p27(KIP1)
Conclusions-Our
The authors investigated whether different campus environment factors were related to eating disorder symptomatology at two distinctly different colleges. The first campus was conservative, placing an emphasis on appearance and dress, whereas the second campus was liberal, placing an emphasis on political activism and intellectual talent. As hypothesized, the two schools did not differ in regard to overall levels of eating disorders, yet different factors were associated with eating disorder symptomatology at each school. Implications for eating disorder interventions on college campuses are discussed.
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