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机构地区:[1]河北医科大学基础医学研究所生化研究室,石家庄050017
出 处:《中国生物化学与分子生物学报》1999年第6期997-1001,共5页Chinese Journal of Biochemistry and Molecular Biology
基 金:国家自然科学基金;河北省自然科学基金
摘 要:建立主动脉内皮剥脱后血管再狭窄大鼠模型,用Northern 印迹分析、含明胶SDS-PAGE、羟脯氨酸含量测定及流式细胞术动态观察血管再狭窄发生过程中MMP-2基因表达与胶原转换及血管细胞增殖之间的关系.实验结果表明,血管内皮剥脱后,MMP-2基因表达被显著诱导,MMP-2活性及胶原转换明显增高,在第7 d,MMP-2表达活性及胶原合成与降解均达到峰值;第21 d,MMP-2表达恢复正常,胶原合成和降解仍维持在较高水平.流式细胞分析结果显示,血管内皮剥脱后进入增殖状态及发生凋亡的细胞显著增加,增殖细胞所占比例高于凋亡细胞,且两者均随内皮损伤后的时间延长而增加.A rat model of vascular restenosis was established by balloon injury.Using Northern blot analysis,SDS PAGE containing gelatin,hydroxyproline concentration determination and flow cytometry analysis,MMP 2 gene expression,collagen turnover and vascular cell proliferation activity were analyzed during vascular restenosis development.The results showed that MMP 2 gene expression was markedly induced by vascular de endothelialization,then MMP 2 activity and collagen turnover increased obviously.On day 7,MMP 2 gene expression,the collagen synthesis and degradation reached the peaks;On day 21,MMP 2 expression returned to basic level.Cell cycle analysis suggested that the number of proliferating and apoptotic cells increased remarkably during vascular restenosis development.With the extension of the time of endothelial injury,both the proliferating cells and apoptotic cells increased,but the proportion of the former was higher than that of the latter.
关 键 词:血管再狭窄 基因表达 胶原转换 MMP-2 ECM
分 类 号:R543.02[医药卫生—心血管疾病]
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