Journal of Southern Medical University ›› 2015, Vol. 35 ›› Issue (01): 29-.
Previous Articles Next Articles
Online:
Published:
Abstract: Objective To investigate whether high glucose-induced vascular calcification is associated with WNT signalingpathway. Methods An in vitro model of human vascular smooth muscle cell (VSMC) calcification was induced by exposure ofthe cells to high glucose. The expressions of WNT signal molecules and bone-related proteins including Cbfa1, Osx, OCN andBMP2 were analyzed with qRT-PCR, and the cell calcification was assessed by alizarin red staining. The effect of Dkk1, a WNTsignaling inhibitor, on high glucose-induced cell calcification was tested with alizarin red staining and calcium contentanalysis. Results High glucose activated WNT signaling pathway in human VSMCs by up-regulating the expressions of WNTsignal molecules including Wnt3a, Wnt7a, Fzd4 and Wisp1 mRNA by 1.86, 1.68, 2.1, and 2.3 folds, respectively, and bypromoting the phosphorylation of β-catenin (2.70±0.22, P<0.05), a key mediator of WNT signaling pathway. Inhibition of WNTsignaling pathway by Dkk1 attenuated high glucose-induced VSMC calcification and down-regulated the expression ofbone-related proteins Cbfa1, Osx, OCN, and BMP2 by (51±9)%, (58±11)%, (56±10)%, and (62±10)% (P<0.01). Conclusion WNTsignaling pathway is involved in high glucose-induced VSMC calcification.
0 / / Recommend
Add to citation manager EndNote|Ris|BibTeX
URL: https://www.j-smu.com/EN/
https://www.j-smu.com/EN/Y2015/V35/I01/29