Objective. To investigate the role and possible mechanism ofα-Klotho in the calcification and the osteogenic transition of cultured VSMCs.Methods. VSMCs were culturedin vitroand divided into 5 groups, each using a different medium: (1) control; (2)β-GP; (3)β-GP + Klotho; (4)β-GP + LiCl; (5)β-GP + Klotho + LiCl. Calcium deposits were visualized using Alizarin Red S staining. The calcium concentrations were determined by the o-cresolphthalein complexone method. BMP2, Runx2 andβ-catenin levels were estimated by western blotting, and the level ofα-SMA was determined by using immunofluorescence at day 12.Results.β-GP induced an increase in the expression of BMP2, Runx2, andβ-catenin. The calcium content increased, and the expression ofα-SMA decreased. Alizarin Red S staining was positive under the high phosphorus conditions. BMP2, Runx2, andβ-catenin levels and the calcium content decreased when the cells were cultured with rmKlotho; however, the levels of each were upregulated after treatment with the LiCl.Conclusions. Klotho can ameliorate the calcification and osteogenic transition of VSMCs induced byβ-GP. The mechanism of Klotho in preventing calcification in VSMCs may be partially mediated by the inhibition of the Wnt/β-catenin signaling pathway.
Puerarin inhibits vascular smooth muscle cells proliferation induced by fine particulate matter via suppressing of the p38 MAPK signaling pathway
