Objective       To determine the role of peroxisome proliferators activated receptor γ (PPARγ) in calcification of vascular smooth muscle cells (VSMCs) induced by high phosphate.        Methods       Cultured mouse VSMCs were divided into normal phosphate (NP) group and high phosphate (HP

2.6 mmol/L) group

and the effect of HP on VSMCs was observed. Then the VSMCs were divided into NP group

HP (2.6 mmol/L) group

rosiglitazone (RGL

10 μmmol/L) group

and HP+RGL (2.6 mmol/L+10 μmmol/L) group

and the inhibitory effect of PPARγ agonist RGL on the calcification of VSMCs induced with HP was observed. Alizarin red S staining was used to observe HP-induced calcification of VSMCs. Expression level of PPARγ

SM22α

BMP2

and Runx2 were measured by Western blotting.        Results       Compared with the NP group

calcium salt deposition of HP-treated VSMCs was higher (0.08±0.02  vs  0.19±0.03

P0.01)

the expression levels of BMP2 (0.26±0.02  vs  0.74±0.03

P0.01) and Runx2 (0.29±0.03  vs  0.91±0.04

P0.01) were increased significantly

and the expression levels of PPARγ (0.93±0.04  vs 0.58±0.02

P0.05) and SM22α (1.02±0.09  vs  0.77±0.03

P0.05) were decreased significantly. After incubation with RGL

calcium salt deposition of HP-treated VSMCs was reduced (0.19±0.02 vs 0.12±0.03

P0.05)

the expression levels of PPARγ (0.63±0.04  vs 0.85±0.03

P0.05) and SM22α (0.69±0.02 vs 0.99±0.03

P0.01) were markedly elevated

and the expression levels of BMP

(1.02±0.04  vs 0.48±0.05

P0.01) and Runx2 (1.00±0.06 vs 0.67±0.03

P0.01) were dropped markedly.        Conclusion       HP-induced osteoblast differentiation and calcification of VSMCs may be related with the down-regulation of PPARγ

and HP-induced calcification of VSMCs can be inhibited by RGL.