| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Research Abstract |
Four weeks after carotid artery ligation, neointimal formation in smRac1+/- mice was substantially reduced compared to control mice. SmRac1+/- SMCs showed decreased chemotaxis, proliferation with decreased phosphorylation of PAK1, ERK, and reduced ROS production compared to that of control SMCs. Furthermore, the expression of cell cycle-associated genes, such as CyclineA, CyclineE, and CDK4 decreased in SMCs from smRac1+/- mice than that in control mice. Moreover, the expression of SM22, a differentiation marker of smooth muscle and highly expressed in differentiated phenotypes of SMCs, was increased in smRac1+/- mice than that in control mice. These results indicate that SMC Rac1 mediates vessel remodeling after intimal injury through inhibition of SMC migration, proliferation and differentiation. Therapeutic modalities, which target Rac1 in SMCs, therefore, may be beneficial in preventing vascular proliferative diseases.
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