Development of intracellular therapy to induce a regression of coronary arteriosclerotic lesions

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1. In the porcine femoral arteries injured by balloon technique, Rho-kinase was upregulated both at the mRNA and activity levels. The in vivo gene transfer of dominant-negative Rho-kinase (DNRhoK) significantly inhibited the development of the balloon injury-induced vascular lesions.2. The long-term treatment of the porcine coronary artery from the adventitial with MCP-1 and Ox-LDL caused a development of arteriosclerotic lesions (intimal thickening and geometric remodeling). The long-term blockade of Rho-kinase with hydroxyfasudil significantly suppressed the development of those vascular lesions.3. The long-term treatment of the porcine coronary artery from the adventitial with IL-1β caused a development of arteriosclerotic lesions (intimal thickening and geometric remodeling). The long-term blockade of Rho-kinase with hydroxy fasudil caused a regression of those vascular lesions in vivo.4. The in vivo gene transfer of DNRhoK induced a regression of constrictive remo deling in a porcine model with IL-1b/These results indicate that Rho-kinase is substantially involved in the pathog enesis of coronary arteriosclerosis and that the long-term inhibition of the molecule could induce a regression of the arterioclerotic vascular lesions.