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凝血酶激活凝血酶受体引起的一系列细胞事件和内源性PDGF-A，bFGF的产生可能是血管病变发生发展过程中平滑肌细胞增生的重要因素。为进一步阐明血管损伤后平滑肌细胞增生的机理及探索有效治疗途径，针对凝血酶受体基因中一段包括转录起始点，翻译起始点，凝血酶结合和切割位点的序列作为靶序列，构建了凝血酶受体反义RNA重组表达载体pLXSN／ATR，并将其导入凝血酶刺激的动脉平滑肌细胞。结果表明重组基因转染能抑制凝血酶对大鼠平滑肌细胞DNA合成的刺激作用。提示序列特异的凝血酶受体反义重组基因的表达可以抑制凝血酶受体介导的血管平滑肌细胞增生。
A series of cellular events induced by thrombin activation thrombin receptor and the production of endogenous PDGF-A and bFGF may be important factors of smooth muscle cell proliferation during the development of vascular lesions. In order to further elucidate the mechanism of smooth muscle cell proliferation after vascular injury and to explore an effective therapeutic approach, aiming at a sequence of thrombin receptor genes including transcription initiation site, translation initiation site, thrombin binding and cleavage site as a target sequence, a coagulation Enzyme Receptor Anti-sense RNA recombinant expression vector pLXSN / ATR, which was introduced into thrombin-stimulated arterial smooth muscle cells. The results showed that recombinant gene transfection can inhibit thrombin on rat smooth muscle cell DNA synthesis stimulation. Suggesting that the expression of the sequence-specific thrombin receptor antisense recombinant gene can inhibit thrombin receptor-mediated vascular smooth muscle cell proliferation.