Immunohistochemical and molecular biological studies of vascular smooth muscle cell proliferation after coronary stent implantation

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1. Proliferation of vascular smooth muscle cells is the main cause of neointimal thickening after coronary intervention. Coronary stents were implanted 2 weeks after balloon injury of porcine coronary arteries. Stent implanted sites were observed in time-course, and the expression of protein kinase C (PKC) were examined. Newly formed neointima was observed 3 days after stenting and the luminal narrowing was prominent from 7 days. There were infiltrating macrophages around stent struts. Positive immunoreactivities of PKC were seen in the proliferated neointima. Our data suggests that the imvolvement of PKC on the smooth muscle cell proliferation after stent implantation.2. It is reported that vascular endothelial growth factor (VEGF) induces neointimai proliferation. Coronary stents were implanted 2 weeks after balloon injury of porcine coronary arteries, and the expressions of VEGF and fit-1 were observed in time-course. The expressions of VEGF and fit-1 were found in the neointima 7 and 1 4 days after stenting. Strong immunoreactivities were observed around stent strut which macrohpages were infiltrated at 28 days. There were positive immunoreactivities in the endothelial cells 1 4 and 28 days. VEGF shows not only the effect of endothelial cell proliferation but also the effect of VSMC proliferation through fit-1.3. It is reported that Rho kinase (Rho K) is involved in the proliferation of VSMC after coronary intervention. Two weeks after balloon injury of porcine coronary arteries, Y27632, which is an inhibitor of Rho K, was administered through drug delivery catheter. The delivery sites were harvested after 4 weeks, and the expression of Rho K was examined. In ultrasound, neointimai proliferation was inhibited, and the lumen was kept wider in Y27632 group. The expression of Rho K was diminished in immnohistochmistry in Y27632 group. Rho k inhibitor may become a useful tool to prevent restenosis inhibiting neointimal proliferation.