Celastrol Protects TGF-β1-induced Endothelial-mesenchymal Tr
发布时间:2018-03-30 06:41
本文选题:endothelial-mesenchymal 切入点:transition 出处:《Journal of Huazhong University of Science and Technology(Medical Sciences)》2017年02期
【摘要】:The endothelial-to-mesenchymal transition(End MT) in endothelial cells contributes to the development of cardiac fibrosis,ultimately leading to cardiac remodeling.In this study,the effects and molecular mechanisms of celastrol(CEL) on transforming growth factor-β1(TGF-β1)-induced End MT in human umbilical vein endothelial(HUVEC-12) cells were investigated.The presented data demonstrated that CEL significantly blocked the morphology change of HUVEC-12 cells induced by TGF-β1 without cell cytotoxicity.In accordance with these findings,CEL blocked TGF-β1-induced EndM T as evidenced by the inhibition of the mesenchymal markers,including collagen Ⅰ,Ⅲ,α-SMA,fibronectin m RNA expression,and the increase in the m RNA expression of endothelial cell marker CD31.These changes were also confirmed by double immunofluorescence staining of CD31 and vimentin.The in vitro scratch assay showed that CEL inhibited the migration capacity of the transitioned endothelial cells induced by TGF-β1.Further experiments showed that the beneficial effect of CEL on blocking the End MT in HUVEC-12 cells was associated with the suppression of the TGF-β1/Smads signalling pathway,which was also confirmed by the inhibition of its downstream transcription factor snail1,twist1,twist2,ZEB1 and ZEB2.These results indicate that CEL blocks TGF-β1-induced End MT through TGF-β1/Smads signalling pathway and suggest that it may be a feasible therapy for cardiac fibrosis diseases.
[Abstract]:The endothelial-to-mesenchymal transition(End MTL in endothelial cells contributes to the development of cardiac fibrosis this studyto cardiac remodeling.In this students) on transforming growth factor- 尾 1TGF- 尾 transforming growth factor- 尾 1)-induced End in human umbilical umbilical vein endothelial services vein were investigated.The presented data data demonstrated that that significantly significantly blocked blocked blocked significantly significantly significantly blocked significantly blocked significantly significantly blocked blocked blocked significantly blocked blocked endothelial induced induced by without #enGF0# cytotoxicity.In cytotoxicity.In cytotoxicity.In #en4@@. The inhibition of the mesenchymal including collagen 鈪,
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