lncRNA MALAT1 Inhibits Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells by Down-Regulating WNT5A

被引:1
作者
Li, Xiaoliang [1 ]
Xia, Guofeng [1 ]
Xing, Hongmei [2 ]
Tao, Chunsheng [1 ]
Lai, Weiwei [1 ]
Sun, Peifeng [1 ]
机构
[1] 971 Hosp Navy Chinese PLA, Dept Orthoped, Qingdao 266071, Shandong, Peoples R China
[2] Shandong Univ Tsingtao, Qilu Hosp, Dept Med Imaging, Shandong 266071, Peoples R China
关键词
lncRNA MALAT1; WNT5A; Osteoporosis; LONG NONCODING RNA; SIGNALING PATHWAY; EXPRESSION; MICRORNAS; CANCER; OSTEOPOROSIS; CONTRIBUTES; PROGRESSION; GROWTH;
D O I
10.1166/jbt.2019.2167
中图分类号
Q813 [细胞工程];
学科分类号
摘要
ncRNA involves in osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). WNT5A participates in the growth and development of osteogenic differentiation. This study aims to investigate whether lncRNA MALAT1 regulates BMSCs osteogenesis through WNT5A. qRT-PCR was done to detect the lncRNA MALAT1 level and osteogenic markers in osteoporosis patients and control groups. The above markers and WNT5A protein levels were detected by Western blot. The degree of osteogenic differentiation was detected by ALP activity assay and ALP staining. The differentiation ability of BMSCs after lncRNA MALAT1 overexpression was detected by ARS staining. The binding site of lncRNA MALAT1 to WNT5A was determined by dual luciferase reporter assay. lncRNA MALAT1 expression was higher in patients with osteoporosis, and decreased significantly with increased osteogenic induction. Overexpression of lncRNA MALAT1 in BMSCS reduced WNT5A level, while interference with lncRNA MALAT1 increased WNT5A levels. In cells with overexpression of lncRNA MALAT1, transfection of si-WNT5A can significantly downregulate the RUNX2, OSX, ALP, OCN, OPN, and COL1A1, thereby inhibiting osteogenic differentiation, interfering with the regulation of WNT signaling pathway and regulating BMSCs osteogenic differentiation. lncRNA MALAT1 and WNT5A can regulate BMSCs osteogenesis, thus accelerating the progression of osteoporosis.
引用
收藏
页码:1520 / 1527
页数:8
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