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See related article, pages 1192–1200 Vascular smooth muscle (VSMC) migration, proliferation, and hypertrophy following physical, chemical, or biological injury are key events in the onset and progression of vascular proliferative disorders, such as atherosclerosis, postangioplasty stenosis, venous bypass graft failure, and transplantation. Under normal conditions, VSMCs exist in a quiescent state of growth that supports contractile function and structural and functional integrity of the vascular wall. Vascular injury disrupts critical cell-cell and cell-matrix interactions, leading to activation of VSMCs. The activated VSMC phenotype is characterized by gradual loss of differentiated characteristics, increased response to chemotactic agents, and uncontrolled proliferation. Not surprisingly, the quest for molecular triggers of VSMC proliferation led investigators to studies of cell cycle control proteins and mitogenic signaling within the vascular wall. Of note are seminal studies examining the signaling cascades of platelet-derived growth factor1,2 and various protooncogenes, including myb ,3,4 myc ,5,6 and H-ras .7,8 H-RAS quickly emerged as a critical convergence point in VSMC mitogenic signaling and was identified as a putative target for pharmacological intervention in vascular proliferative disorders.9H - and K-ras were first identified as viral oncogenes in Harvey and Kirsten rat sarcomas, respectively.10 Subsequent studies identified a third member, N-ras , as a protooncogene present in various tumor cell lines.11 Studies of the cellular viral ras oncogene counterparts led to the identification of ras protooncogenes as TATA-less, GC-rich genes that encode for 21-kDa proteins with homology to the α subunit of G proteins.12 p21RAS binds guanine nucleotides and possesses intrinsic GTPase activity,13 and mutations at …

H-RAS Controls Phenotypic Profiles of Vascular Smooth Muscle Cells and the Pathogenesis of Vascular Proliferative Disorders