β-catenin在lα,25-(OH)2D3调控小鼠体外破骨细胞形成中的作用

Role of β-catenin in mice osteoclastogenesis controlled by lα,25-(OH)2D3 in vitro

旨在探究β-catenin在lα,25-(OH)2D3调控小鼠体外破骨细胞(osteoclast,OC)形成中的作用。体外诱导小鼠OC形成,添加1α,25-(OH)2D3观察其对OC形成及β-连环蛋白(β-catenin)表达的影响;敲低β-catenin进一步观察1α,25-(OH)2D3对OC形成的影响。结果显示,1α,25-(OH)2D3极显著(P<0.01)抑制体外培养小鼠OC形成和骨吸收活性。敲低β-catenin,OC数量及OC形成标志物基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)蛋白和激活T-细胞核因子1(nuclear factor of activated T cells,cytoplasmic 1,Nfatc1)mRNA表达显著(P<0.05)升高。1α,25-(OH)2D3可促进OC形成过程中β-catenin基因Ctnnb1 mRNA的表达,但敲低β-catenin基因,1α,25-(OH)2D3仍可抑制OC形成。试验表明,β-catenin可抑制体外培养OC形成,但对1α,25-(OH)2D3抑制OC形成无影响。

To investigate the role ofβ-catenin in mice osteoclastogenesis controlled by lα,25-(OH)2D3 in vitro,mice osteoclasts(OC)were induced in vitro and treated by 1α,25-(OH)2D3.The number of OC and the expression ofβ-catenin were detected before and afterβ-catenin knocking-down.The results showed that,1α,25-(OH)2D3 significantly inhibited mice OC formation and bone resorption activity in vitro.OC number,the expression of matrix metalloproteinase-9(MMP-9)protein and nuclear factor of activated T cells,cytoplasmic 1(Nfatc1)mRNA were upregulated afterβ-catenin knocking-down.During OC formation,1α,25-(OH)2D3 upregulated the expression ofβ-catenin gene Ctnnbl mRNA.However,when knocking downβ-catenin gene,1α,25-(OH)2D3 can still significantly inhibit OC formation.In conclusion,β-catenin inhibited mice OC formation in vitro,but had no effect on OC formation inhibited by 1α,25-(OH)2D3.