Effect of SOX9 on Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells Through WNTβ/Catenin Pathway

被引:0
作者
Yang, Qing [1 ]
Li, Cheng [2 ]
Yan, Manli [3 ]
Fang, Chunhua [4 ]
机构
[1] Jianghan Univ, Affiliated Hosp 2, Dept Orthoped, Wuhan 430050, Hubei, Peoples R China
[2] Wuhan 1 Hosp, Dept Crit Care Med, Wuhan 430022, Hubei, Peoples R China
[3] Wuhan Hanyang Dist Disabled Persons Federat, Wuhan 430050, Hubei, Peoples R China
[4] Jianghan Univ, Affiliated Hosp 2, Dept Digest Med, Wuhan 430050, Hubei, Peoples R China
关键词
SOX9; BMSCs; Proliferation; Wnt beta/Catenin Signaling Pathway; Osteogenic Differentiation;
D O I
10.1166/jbt.2019.2140
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Bone marrow mesenchymal stem cells (BMSCs) can be differentiated into different types of cells. SOX9 involves in the development and progression of various diseases. Our study aims to assess SOX9's effect on osteogenic differentiation of BMSCs and its related regulatory mechanisms. Rat BMSCs were isolated and randomly divided into control group, SOX9 group and SOX9 siRNA group, which was transfected with pcDNA-SOX9 plasmid or SOX9 siRNA respectively followed by analysis of SOX9 expression by Real time PCR, cell proliferation by MTT assay, Caspase3 and ALP activity, GSK-3 beta expression and Wnt beta/Catenin Signaling pathway protein expression by Western blot, and expression of osteogenic genes Runx2 and BMP-2 by Real time PCR. Transfection of pcDNA-SOX9 plasmid into BMSCs significantly inhibited cell proliferation, promoted Caspase3 activity, decreased ALP activity and downregulated Runx2 and BMP-2, increased GSK-3 beta expression and decreased Wnt beta/Catenin expression protein expression (P < 0.05). SOX9 siRNA transfection significantly promoted cell proliferation, inhibited Caspase3 activity, increased ALP activity and upregulated Runx2 and BMP-2, downregulated GSK-3 beta and increased Wnt beta/Catenin expression. SOX9 regulates BMSCs proliferation and osteogenic differentiation through Wnt beta/Catenin signaling pathway.
引用
收藏
页码:1429 / 1434
页数:6
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