滋养细胞诱导肾小球内皮细胞损伤的机制及细胞因子干预靶点研究  

Mechanism of glomerular endothelial cell injury induced by trophoblast cell and cytokine target involved in protective effects of such injury.

作　　者：赵君[1] 刘海意[1] 杜慧[1] 李宇琪[1] 乔福元[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院妇产科,湖北武汉430030

出　　处：《中国优生与遗传杂志》2011年第7期66-68,共3页Chinese Journal of Birth Health & Heredity

基　　金：湖北省科技计划自然科学基金项目(2009CDB023)

摘　　要：目的通过研究病理状态的滋养细胞与肾小球内皮细胞共培养后细胞的形态变化、ET-1表达改变及VEGF干预效果,探讨子痫前期肾小球内皮细胞的损伤机制及针对该损伤的保护机制。方法将紫外线、水浴分别诱导凋亡、坏死的滋养细胞与肾小球内皮细胞共培养,荧光显微镜下观察细胞形态,real-time PCR检测ET-1mRNA;;表达,同时给予VEGF干预,琼脂糖凝胶电泳进行PCR产物验证。结果肾小球内皮细胞吞噬死亡的滋养细胞后ET-1mRNA;;表达量增加,应用VEGF干预后ET-1mRNA;;表达量下降。结论在子痫前期中,肾小球内皮细胞可能是通过吞噬死亡的滋养细胞引起ET-1的表达变化,进而发生损伤。VEGF可以抑制ET-1的表达从而改善该损伤。Objective： To investigate the changes in cells morphology,ET-1 expression and interference effect of VEGF after co-culture of trophoblast cell and glomerular endothelial cell,in order to further study the dysfunctional and protective mechanism of glomerular endothelial cell in preeclampsia.Methods： Both apoptotic and necrotic trophoblasts and glomerular endothelial cells were mixed and cultured for 24 hours.Fluorescence microscope demonstrated cells morphology.The ET-1 gene expression was examined by fluorescent real-time PCR and was inhibited by VEGF.The products of PCR amplification were detected by agarose gel electrophoresis.Results： Through phagocytosed death trophoblasts,endothelial cells induced increased ET-1 expression.ET-1 level significantly reduced in the VEGF intervention group.Conclusion： Glomerular endothelial cells,which phagocytosed death trophoblasts,may be the important factor of high expression of ET-1.And,ET-1 may be the key factor to contribute to endothelial cell dysfunction in preeclampsia.VEGF may be improve endothelial cell injury by inhibiting ET-1 expression.

关 键 词：滋养细胞 肾小球内皮细胞 ET-1 VEGF 

分 类 号：R714.245[医药卫生—妇产科学]