人脐静脉血管内皮细胞缺氧复氧损伤时黏结合蛋白多糖1及细胞外信号调节酶表达与肝素酶Ⅰ的调节  

Effects of heparinase Ⅰ on syndcan-1 and extracelluar signal regulated kinase expression in human umbilical vein endothelial cells following hypoxia/reoxygenation

作　　者：罗海彦[1] 胡长林[1] 

机构地区：[1]重庆医科大学附属第二医院神经病学研究室,重庆市400010

出　　处：《中国组织工程研究与临床康复》2010年第11期1995-1999,共5页Journal of Clinical Rehabilitative Tissue Engineering Research

基　　金：重庆市卫生局渝卫科教基金项目(2005-31);重庆医科大学科技基金(XB-0518)~~

摘　　要：背景:研究发现肝素酶可以促使肿瘤细胞的syndecan-1脱落,而且低氧增加的巨噬细胞运动也可能与硫酸已酰肝素蛋白多糖的生物合成调节相关。目的:观察肝素酶Ⅰ对缺氧复氧损伤人脐静脉血管内皮细胞黏结合蛋白多糖1及细胞外信号调节酶的调节作用。方法:采用缺氧复氧处理肝素酶Ⅰ预培养的人脐静脉血管内皮细胞,用免疫组织化学、RT-PCR及western blot检测人脐静脉血管内皮细胞细胞黏结合蛋白多糖1、ERK2的表达。结果与结论:单纯缺氧复氧后人脐静脉血管内皮细胞的黏结合蛋白多糖1和ERK2表达轻度上调。缺氧复氧处理肝素酶Ⅰ预培养人脐静脉血管内皮细胞的黏结合蛋白多糖1和ERK2明显上调,与单纯缺氧复氧处理人脐静脉血管内皮细胞相比差异有显著性意义。黏结合蛋白多糖1与ERK2上调表达成正相关。结果表明,黏结合蛋白多糖1和细胞外信号调节酶参与了人脐静脉血管内皮细胞缺氧复氧损伤的病理生理过程,肝素酶Ⅰ可能通过调节黏结合蛋白多糖1来影响细胞外信号调节酶的表达。BACKGROUND： Heparinase can induce syndecan-1 shedding from tumor cells, and macrophage motion may correlate with biosynthesis regulation of heparan sulfate proteoglycan. OBJECTIVE： To investigate the effects of heparinaseⅠon syndecan-1 and extracelluar signal regulated kinase 2 （ERK2） in human umbilical vein endothelial cells （HUVECS） with hypoxia/reoxygenation injury. METHODS： heparinaseⅠ-precultured HUVECS were treated with hypoxia/reoxygenation. Immunohistochemistry staining, RT-PCR and western blot were applied to detect HUVECS syndecan-1 and ERK2 expression. RESULTS AND CONCLUSION： Expression of syndecan-1 and ERK2 was increased in HUVECS following hypoxia/reoxygenation treatment. HeparinaseⅠ significantly upregulated the expression of syndecan-1 and ERK2 in HUVECS with hypoxia/reoxygenation treatment. Syndecan-1 and ERK2 expression was positively related. Results show that syndecan-1 and ERK2 participate the pathophysiology of HUVECs hypoxia/reoxygenation injury. HeparinaseⅠ influences ERK2 expression by regulating syndecan-1.

关 键 词：肝素酶Ⅰ 黏结合蛋白多糖1 细胞外信号调节酶 缺氧/复氧损伤 人脐静脉血管内皮细胞 

分 类 号：R318[医药卫生—生物医学工程]