The effect of TGF-β/ILK pathway in endothelial-mesenchymal transition induced by parathyroid hormone in human vascular endothelial cells
10.3969/j.issn.1671-8348.2018.16.007
- VernacularTitle:TGF-β/ILK信号通路在甲状旁腺激素诱导血管内皮细胞向间质细胞转化中的作用
- Author:
Ning LI
1
;
Keqin ZHANG
;
Kanfu PENG
Author Information
1. 重庆大学附属中心医院/重庆市急救医疗中心/重庆市第四人民医院内分泌肾内科 400014
- Keywords:
parathyroid hormone;
vascular endothelial cells;
endothelial-mesenchymal transition;
transforming growth factor-β;
integrin-linked kinase
- From:
Chongqing Medicine
2018;47(16):2140-2143
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the molecular mechanism of endothelial-mesenchymal transition (EndMT) induced by uremic toxin,parathyroid hormone (PTH),in vascular endothelial cells.Methods PTH (1 × 10-8 mol/L) was used to induce EndMT in human aortic endothelial cells (HAECs).TGF-β signaling inhibitor,including SB431542 and pirfenidone (PFD),and integrin-linked kinase (ILK) inhibitor Cpd22 were used to investigate the potential mechanism of EndMT induced by PTH in HAECs.Then the vascular endothelial cell markers VE-cadherin and CD31,and the mesenchymal marker α-SMA were detected by western blot.Results PTH reduced the expression levels of vascular endothelial cell marker CD31 and VE-cadherin (P＜0.05),while significantly increased the expression level of fiber cell marker α-SMA(P＜0.05).Furthermore,the TGF-βsignaling inhibitors (SB431542 and PFD) and ILK inhibitor (Cpd22) were able to partially reverse the EndMT induced by PTH in HAECs,which reversed the effect of PTH on reducing vascular endothelial cell marker expression and increasing fiber cell marker expression.Conclusion PTH could induce EndMT in HAECs via TGF-β/ILK pathway.
