CAJ | 학술논문

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枪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,与单纯缺氰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.
배경:연구발현간소매가이촉사종류세포적syndecan-1탈락,이차저양증가적거서세포운동야가능여류산이선간소단백다당적생물합성조절상관.목적:관찰간소매Ⅰ대결양복양손상인제정맥혈관내피세포점결합단백다당1급세포외신호조절매적조절작용.방법:채용결양복양처리간소매Ⅰ예배양적인제정맥혈관내피세포,용면역조직화학、RT-PCR급western blot창측인제정맥혈관내피세포세포점결합단백다당1、ERK2적표체.결과여결론:단순결양복양후인제정맥혈관내피세포적점결합단백다당1화ERK2표체경도상조.결양복양처리간소매예배양인제정맥혈관내피세포적점결합단백다당1화ERK2명현상조,여단순결청복양처리인제정맥혈관내피세포상비차이유현저성의의.점결합단백다당1여ERK2상조표체성정상관.결과표명,점결합단백다당1화세포외신호조절매삼여료인제정맥혈관내피세포결양복양손상적병리생리과정,간소매Ⅰ가능통과조절점결합단백다당1래영향세포외신호조절매적표체.
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 heparinase Ⅰ on syndecan-1 and extracelluar signal regulated kinase 2(ERK2)in human umbilical vein endothelial cells(HUVECS)with hypoxia/reoxygenation injury.METHODS:heparinase Ⅰ-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.Heparinase Ⅰ 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 Heparinase Ⅰ influences ERK2 expression by regulating syndecan-1.