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目的:探讨E1A激活基因阻遏子(CREG)在动脉粥样硬化(AS)发展中的作用。方法:采用Western blot方法检测AS患者血管中CREG表达的变化。用高脂饲料喂养兔子的方法模拟AS的自热进程,观察血管的形态学变化。用免疫组化染色法检测血管平滑肌细胞(VSMCs)增殖及CREG、SMα-actin和SM MHC表达的变化。结果:在AS患者的血管中,CREG的表达明显下调。在动物模型中,以高脂饲料喂养兔1个月时,血管内皮出现不光滑、内膜增厚,中膜VSMCs出现表型转化,收缩蛋白SMα-actin和SM MHC的表达开始下降,细胞出现增生,此时CREG的表达也开始下调。以高脂饲料喂养兔2个月时,可见内皮有中断、破损现象,内膜增厚明显,增殖细胞核抗原(PCNA)表达阳性的细胞明显增多,CREG的表达进一步下调,VSMCs中的收缩蛋白也进一步下降。结论:在AS进程中,血管中膜的VSMCs由收缩表型向合成表型转化,细胞增生活跃、分化减弱,CREG随着AS的发展,在VSMCs中的表达逐步下降,提示CREG作为维持VSMCs分化的蛋白与AS的发生发展密切相关。
Objective: To investigate the role of E1A-activated gene repressor (CREG) in the development of atherosclerosis (AS). Methods: The changes of CREG expression in blood vessels of AS patients were detected by Western blot. Rabbits were fed with high-fat diet to simulate the autothermic process of AS and observe the morphological changes of blood vessels. The changes of proliferation, SMα-actin and SM-MHC expression in vascular smooth muscle cells (VSMCs) were detected by immunohistochemistry. Results: In patients with AS, the expression of CREG was significantly down-regulated. In the animal model, feeding rabbit with high-fat diet for 1 month resulted in a smoother endothelium and thickening of the intima, and a phenotypic transformation of VSMCs in mesangial cells. Expression of contractile proteins SMα-actin and SM MHC began to decline, and cells appeared Proliferation, CREG expression began to decline at this time. When fed with high-fat diet for 2 months, the endothelial cells were disrupted and damaged, and the intimal thickening was obvious. The number of PCNA positive cells was significantly increased and the expression of CREG was further down-regulated. The contractile proteins in VSMCs Further decline. CONCLUSIONS: In VSMCs, the VSMCs of VSMCs from the contractile phenotype to the synthetic phenotype are transformed, the cell proliferation is active and differentiation is weakening. The expression of CREG gradually decreases in VSMCs with the development of AS, which suggests that CREG, The protein is closely related to the occurrence and development of AS.