• Original article (Basic research) • Previous Articles     Next Articles

Inhibition of advanced glycation end products-induced endothelial cells calcification by silencing S100A4

YUE Wen-heng, LI Na, WANG Qin-qin, LIANG Chun   

  1. Department of Cardiology, Changzheng Hospital, Shanghai Second Military Medical University, Shanghai 200003, China
  • Online:2016-07-28 Published:2016-08-31
  • Supported by:

    National Natural Science Foundation of China,81270405


Objective To investigate the effects of silencing the S100A4 gene of human umbilical vein endothelial cells (HUVECs) on advanced glycation end products (AGE)-induced vascular calcification. Methods Recombinant viruses were transfected into HUVECs cultured in vitro to inhibit the expression of S100A4. Transfected HUVECs were stimulated with AGE to construct a diabetic cell model. The calcification of HUVECs was assessed by measuring the calcium ion level in cells, detecting the expression levels of matrix Gla protein (MGP), bone morphogenetic protein-2 (BMP2), and alkaline phosphatase (ALP) with Western blotting, as well as alizarin red staining. Results The concentration of calcium ion in HUVECs was significantly increased by the stimulation of AGE. Silencing of S100A4 could reverse the AGE-induced high expression of MGP and AGE-induced low expressions of BMP2 and ALP (P<0.01 for all) and significantly reduce the area of alizarin red staining. Conclusion Silencing of S100A4 with recombinant viruses can reduce the calcification of HUVEC induced by AGE. S100A4 may be a potential target for the treatment of vascular calcification in diabetic patients.

Key words: S100A4, endothelial cells, advanced glycation end products, calcification