【摘要】 目的探讨klotho对高磷诱导的HASMCs钙化的作用机制。方法建立HASMCs钙化模型,将其分4组:正常磷浓度组(I)、高磷浓度培养组(Ⅱ)、正常磷浓度+klotho基因转染组(Ⅲ)、高磷浓度+klotho基因转染组(Ⅳ)。培养9 d后用茜素红染色观察细胞钙化程度,测定细胞外基质钙含量。检测各组细胞ALP、OPG、OPN、Runx2、β-catenin等蛋白的表达。结果Ⅱ组钙盐沉积明显,细胞外基质钙含量、ALP、Runx2及β-catenin蛋白表达明显高于其他各组(P<0.05),OPG及OPN蛋白表达明显低于其他各组(P<0.05)。结论 klotho通过下调Wnt/β-catenin信号通路可抑制高磷诱导的HASMCs钙化。更多还原

【Abstract】 Objective To explore the mechanism of klotho on hyperphosphate-induced calcification of HASMCs. Methods The calcification model of HASMCs was established and divided into 4 groups: normal phosphorus concentration group(I), high phosphorus concentration culture group(Ⅱ), normal phosphorus concentration+klotho gene transfection group(Ⅲ), and high phosphorus concentration+klotho Gene transfection group(Ⅳ). After 9 days of culturing, the degree of cell calcification was observed with alizarin red staining, and the extracellular matrix calcium content was determined. The expression of ALP, OPG, OPN, Runx2, β-catenin, and other proteins in cells of each group was detected. Results Calcium salt deposition was obvious in group Ⅱ. The extracellular matrix calcium content,ALP,Runx2 and β-catenin protein expression were significantly higher than other groups(P<0.05). The OPG and OPN protein expression were significantly lower than other groups(P<0.05). Conclusion Klotho can inhibit hyperphosphate-induced calcification of HASMCs by down-regulating Wnt/β-catenin signaling pathway.更多还原