Down-regulation of LECT2 promotes osteogenic differentiation of MSCs via activating Wnt/β-catenin pathway

被引:19
|
作者
Xu, Zhonghua [1 ]
He, Jin [1 ]
Zhou, Xindie [2 ]
Zhang, Yi [2 ]
Huang, Yong [2 ]
Xu, Nanwei [2 ]
Yang, Haoyu [3 ]
机构
[1] Jiangsu Univ, Dept Orthoped, Jintan Hosp, Changzhou 213200, Peoples R China
[2] Nanjing Med Univ, Dept Orthoped, Affiliated Changzhou 2 Peoples Hosp, Changzhou 213003, Peoples R China
[3] Soochow Univ, Dept Orthoped, Wuxi 9 Peoples Hosp, Wuxi 214000, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Osteoporosis; Osteogenic differentiation; Mesenchymal stem cells; Wnt/beta-catenin; MESENCHYMAL STEM-CELLS; TUMOR-GROWTH; BONE; PROTEIN; ADIPOGENESIS; OSTEOPOROSIS; OSTEOBLAST;
D O I
10.1016/j.biopha.2020.110593
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Osteoporosis is a result of the imbalance between osteoblasts and osteoclasts quantities, which is closely correlated with osteogenic differentiation (OD). Leucocyte cell-derived chemotaxin 2 (LECT2) has been reported as a regulatory factor in some chronic diseases such as hepatitis through mediating downstream target gene beta-catenin. Additionally, Wnt/beta-catenin is also the crucial modulatory signal pathway in OD. Mesenchymal stem cells (MSC) is a kind of mesodermal stem cells; its differentiation direction is discovered affected by Wnt/beta-catenin. However, the function of LECT2 in osteoporosis still remains exploration, which encourages us to lucubrate its functional effect in regulating the OD of MSCs. In this study, we found that LECT2 was expressed at low level in MSCs with osteogenic differentiation, and knockdown of LECT2 would activate Wnt/beta-catenin pathway and therefore promoting OD in MSCs. It is the first time to report that LECT2 participates in regulating OD via mediating Wnt/beta-catenin. Our discovery would affirmatively help provide a novel strategy for the diagnosis and therapy methods for osteoporosis.
引用
收藏
页数:10
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