Small nuclear ribonucleoprotein polypeptide N (Sm51) promotes osteogenic differentiation of bone marrow mesenchymal stem cells by regulating Runx2

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• 作者：Fanbiao Meng ; Liangliang Xu ; Shuo Huang ; Yang Liu ; Yonghui Hou…
• 关键词：KeywordMesenchymal stem cells ; Osteogenesis ; Sm51 ; Runx2
• 刊名：Cell and Tissue Research
• 出版年：2016
• 出版时间：October 2016
• 年：2016
• 卷：366
• 期：1
• 页码：155-162
• 全文大小：2,550 KB
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Human Genetics
  Proteomics
  Molecular Medicine
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-0878
• 卷排序：366

文摘

Small nuclear ribonucleoprotein-associated polypeptide N mutation in mice is associated with short limbs and lower bone mineral density, yet the role of Sm51 in MSC differentiation to osteoblasts is not known. In the present study, we investigate the role of Sm51 in regulating osteoblastic differentiation of bone marrow-derived mesenchymal stem cells (BM-MSCs). Stable overexpression of Sm51 in rat and human BM-MSCs (Sm51-MSCs) significantly enhanced their osteogenic differentiation potential compared to untransfected cells. Under osteogenic induction, Sm51-MSCs had higher alkaline phosphatase (ALP) activity and mineralization ability; the expression of osteogenic genes such as runt-related transcription factor 2 (Runx2), osteocalcin, osteopontin, ALP and type I collagen was significantly upregulated compared to the control BM-MSCs. Furthermore, we show that Sm51 overexpression upregulated Runx2 expression at both the RNA and protein level; Sm51 could bind to Runx2 RNA and regulate its expression. Finally, knocking down Runx2 abolished the promoting effects of Sm51 on osteogenesis in BM-MSCs. These results demonstrate that Sm51 plays an important role in regulating osteogenic differentiation of MSCs through increasing Runx2 expression and that Sm51 may be a potential new therapeutic target for promoting bone formation.