摘要
传统观点认为,肾小球内凝血导致慢性进行性肾损伤的主要机制是微血栓形成引起肾小球缺血性损伤。近年来作者采用细胞生物学方法,观察了活化凝血因子凝血酶和纤维蛋白对肾小球内皮细胞(GEC)和系膜细胞的直接影响,发现凝血酶可以诱导GEC增殖、细胞外基质降解增加以及细胞脱壁;纤维蛋白可以支持GEC铺展、增殖,并可以诱导GEC单层结构破坏和血管样结构形成,同时可以上调胞间粘附分子-1(ICAM-1)的表达。凝血酶还可以促进系膜细胞增殖、表达ICAM-1、纤溶酶原激活物抑制物-1(PAI-1)、基质金属蛋白酶-2(MMP-2)及基质金属蛋白酶-9(MMP-9)。据此认为,肾小球内凝血可以通过活化凝血因子对GEC和系膜细胞的直接作用,转化为炎症反应,并影响细胞外基质的重塑。
Traditionally, it was believed that renal injury caused by intraglomerular coagulation could be attributed to glomerular ischemia due to microthrombosis. Using cellular biological methods, we observed the effects of activated coagulation factors including thrombin and fibrin on glomerular endothelial cells(GEC) and mesangial cells. Results showed that thrombin induced GEC proliferation, extracellular matrix degradation, as well as GEC detachment; fibrin not only supported GEC attachment, spreading, and proliferation, induced GEC monolayer disorganization and capillary structure formation, but also promoted ICAM1 expression. Thrombin promoted proliferation of mesangial cells, and enhanced the expression of ICAM1, MMP2, and MMP9 in mesangial cells. It is concluded that intraglomerular coagulation might shift to inflammatory reaction and influence the remodelling of extracellular matrix by the direct effect of activated coagulation factors on GEC and mesangial cells.
出处
《解放军医学杂志》
CAS
CSCD
北大核心
1999年第3期157-159,共3页
Medical Journal of Chinese People's Liberation Army