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通过免疫组织化学和电子显微镜的方法鉴定了原代培养的人腹主动脉平滑肌细胞,并且研究全反式维甲酸对其增殖的影响,发现atRA使SMC的增殖速度变慢,经atRA处理的细胞中cyclinD1,CDK4的表达分别降低了39％和38％,c-myc基因的表达水平降低了43.6％,而平滑肌特异的α-actin的表达不受影响。说明atRA可能通过降低细胞中c-myc,CDK4,cy-clinD1的基因表达水平而抑制SMC的生长,但并不引起SMC分化。atRA抑制SMC增殖可能为临床上探索atRA治疗SMC增生性疾病如动脉粥样硬化提供一些理论依据。
Primary cultured human aortic smooth muscle cells were identified by immunohistochemistry and electron microscopy and the effect of all-trans retinoic acid on their proliferation was examined. AtRA was found to slow SMC proliferation and atRA-treated cells The expression of cyclinD1 and CDK4 decreased by 39% and 38%, while the expression of c-myc gene decreased by 43.6%, while the smooth muscle-specific α-actin expression was not affected. AtRA may inhibit the growth of SMC by reducing the gene expression of c-myc, CDK4 and cy-clinD1 in the cells, but not SMC differentiation. Inhibition of SMC proliferation by atRA may provide some theoretical basis for the clinical exploration of atRA for the treatment of SMC proliferative diseases such as atherosclerosis.