The effect and underlying mechanism of miRNA-506 regulating TGF-β1-induced endothelial-mesenchymal transition of human aortic endothelial cell lysates / 中国医师杂志

ABSTRACT

Objective To investigate the effect and the underlying mechanism of miRNA (miR)-506 regulating transforming growth factor-β1 (TGF-β1)-induced endothelial-mesenchymal transition of human aortic endothelial cell lysates.Methods In this study,miR-506 and inhibitory members of the ASPP family (iASPP) were selected as the study objects.First,the expression of miR-506 in human aortic endothelial cell lysates (HAEC) lysate was detected under different concentrations of TGF-β1.The expression of platelet endothelial cell adhesion molecule-1 (CD31),endothelium-cadherin (VE-cadherin),fibroblastspecific protein-1 (FSP1),α-smooth muscle actin (α-SMA) and N-cadherin was determined after miR-506 mimics/mimic negative control (NC) transfection into HAEC treated with or without TGF-β1.Then the expression levels of iASPP in miRNA-506 mimics/mimic NC-transfected HAECs treated with or without TGF-β1 were determined.Finally,the protein expression of CD31,VE-cadherin,FSP1 and α-SMA in HAEC transfected with miR-506 mimics/mimic NC was determined after iASPP overexpression.Results TGF-β1 can induce human aortic endothelial cell mesenchymal transition,down-regulate CD31 and VE-cadherin expression while up-regulate FSP1,α-SMA and N-cadherin expression;TGF-β1 inhibited miR-506 expression,promoted iASPP expression;miR-506 transfection into HAECs up-regulated CD31 and VE-cadherin expression while up-regulate FSP1,α-SMA and N-cadherin expression;miR-506 could downregulate the expression of iASPP;the overexpression of iASPP increased the expression of FSP1,α-SMA and N-cadherin,down-regulated CD31 and VE-cadherin and promoted the transformation of human aortic endothelial cells.Conclusions The transfection of iASPP plasmid promoted the endothelial-mesenchymal transition of human aortic endothelial cell lysates.The transfection of miR-506 inhibited the expression of iASPP and inhibited the endothelial-mesenchymal transition of human aortic endothelial cell lysates induced by TGF-β1.