放射治疗支架内再狭窄诱导平滑肌细胞凋亡的分子机制  

Molecular mechanism of vascular smooth muscle cells apoptosis induced by in-stent restenosis during radiation

作　　者：余小平[1] 张斌[1] 曲环[1] 杨海涛[1] 王纯[1] 董会奕[1] 

机构地区：[1]北京大学深圳医院心内科,广东深圳518036

出　　处：《中国老年学杂志》2006年第5期644-646,共3页Chinese Journal of Gerontology

摘　　要：目的研究支架内再狭窄部位平滑肌细胞(rVSMC)凋亡水平改变的机制,并探讨放疗诱导细胞凋亡的调控途径。方法50例支架术后再狭窄患者,取其斑块标本,检测p53、p21和Cyclin D1的表达水平,并与正常冠脉血管平滑肌细胞(nVSMC)进行比较。结果rVSMC中,p53和p21的表达略低于正常细胞,分别为80%和75%左右(P<0.05);Cyclin D1则达到了正常细胞的2倍以上(P<0.01)。照射后,rVSMC和nVSMC的细胞凋亡均有上升(P<0.01),且rVSMC的上升幅度大于nVSMC(P<0.05);而两组细胞中p53、p21和Cyclin D1的表达水平基本相同。结论rVSMC中p53、p21和Cyclin D1的表达水平发生改变,导致细胞凋亡减少,是发生支架内再狭窄的重要原因。放疗可改变rVSMC中各凋亡相关分子的表达,诱导细胞凋亡。Objective To investigate the molecular mechanism of apoptosis in vascular smooth muscle cells （VSMCs） at in-stent restenosis sites and to explore the regulative pathway induced by radiation. Methods 50 patients with restenosis after in-stenting were sampled （rVSMCs） to detect the expression of p53, p21 and cyclin D1 and to compare with normal specimens （nVSMCs）. Results Expression of p53 and p21 in rVSMCs was lower than that in controls, 80% and 75% respectively （P 〈0.05）, however, the level of cyclin D1 was more than 2-fold higher than normal controls （P 〈 0.01 ）. After radiation, the apoptosis of rVSMCs and nVSMCs both increased （P 〈 0.01 ） and the change in rVSMCs was greater than that in nVSMCs （ P 〈 0.05 ）. While the expressions of p53, p21 and cylcin D1 were basically same between two groups. Conclusions The changed expression level of p53, p21 and cyclin D1 in rVSMCs could induce the decreased cell apoptosis, which may be the important cause resulting in in-stent restenosis. Radiation could alter expressions of molecular related apoptosis and induce cell apoptosis.

关 键 词：支架内再狭窄 血管平滑肌细胞 凋亡 放射治疗 

分 类 号：R871.1[医药卫生—运动医学]