The LncRNA ZBED3-AS1 induces chondrogenesis of human synovial fluid mesenchymal stem cells

Human synovial fluid-derived mesenchymal stem cells (SFMSCs) have great potential for cartilage induction and are promising for cell-based strategies for articular cartilage repair. Many long non-coding RNAs (lncRNAs) regulate chondrogenesis of MSCs. We hypothesized that the divergent lncRNA ZBED3-A...

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Published inBiochemical and biophysical research communications Vol. 487; no. 2; pp. 457 - 463
Main Authors Ou, Farong, Su, Kai, Sun, Jiadong, Liao, Wenting, Yao, Yu, Zheng, Youhua, Zhang, Zhiguang
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 27.05.2017
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Summary:Human synovial fluid-derived mesenchymal stem cells (SFMSCs) have great potential for cartilage induction and are promising for cell-based strategies for articular cartilage repair. Many long non-coding RNAs (lncRNAs) regulate chondrogenesis of MSCs. We hypothesized that the divergent lncRNA ZBED3-AS1, which binds locally to chromatin, could promote the expression of zbed3, a novel Axin-interacting protein that activates Wnt/β-catenin signaling, involved in chondrogenesis. However, the function of ZBED3-AS1 in SFMSCs is unclear. In this study, the expression, biological function, and roles of ZBED3-AS1 in SFMSC chondrogenesis were examined by multilineage differentiation, flow cytometry, and gain-of-function studies. We found that ZBED3-AS1 promotes chondrogenesis. Furthermore, ZBED3-AS1 could directly increase zbed3 expression. Finally, the wnt-inhibitor DKK1 could reverse the stimulatory effect of ZBED3-AS1 on chondrogenesis. These findings demonstrate the role of a new lncRNA, ZBED3-AS1, in SFMSC chondrogenesis and may improve osteoarthritis treatment. •ZBED3-AS1 directly increases zbed3 expression in human synovial fluid-derived MSCs.•A wnt-inhibitor reversed the stimulatory effect of ZBED3-AS1 on chondrogenesis.•A new lncRNA, ZBED3-AS1, promotes SFMSC chondrogenesis via wnt signaling.•ZBED3-AS1 may have therapeutic applications for articular cartilage repair.
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ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2017.04.090