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MiR?483?3p regulates osteogenic differentiation of bone marrow mesenchymal stem cells by targeting STAT1.


ABSTRACT: Osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) is regulated by a variety of intracellular regulatory factors including osterix, runt?related transcription factor 2 (RUNX2), bone morphogenetic proteins and transforming growth factor?. Recent studies have shown that microRNAs (miRs) serve a crucial role in this process. In the present study, miR?483?3p levels were significantly increased during osteogenic differentiation of mouse and human BMSCs. Overexpression of miR?483?3p promoted osteogenic differentiation, whereas inhibition of miR?483?3p reversed these effects. miR?483?3p regulated osteogenic differentiation of BMSCs by targeting STAT1, and thus enhancing RUNX2 transcriptional activity and RUNX2 nuclear translocation. In vivo, overexpression of miR?483?3p using a BMSC?specific aptamer delivery system stimulated bone formation in aged mice. Therefore, the present study suggested that miR?483?3p promoted osteogenic differentiation of BMSCs by targeting STAT1, and miR?483?3 prepresent a potential therapeutic target for age?related bone loss.

SUBMITTER: Xiao Y 

PROVIDER: S-EPMC6797999 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature

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miR‑483‑3p regulates osteogenic differentiation of bone marrow mesenchymal stem cells by targeting STAT1.

Xiao Ye Y   Guo Qi Q   Jiang Tie-Jian TJ   Yuan Ying Y   Yang Li L   Wang Guang-Wei GW   Xiao Wen-Feng WF  

Molecular medicine reports 20190924 5


Osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) is regulated by a variety of intracellular regulatory factors including osterix, runt‑related transcription factor 2 (RUNX2), bone morphogenetic proteins and transforming growth factorβ. Recent studies have shown that microRNAs (miRs) serve a crucial role in this process. In the present study, miR‑483‑3p levels were significantly increased during osteogenic differentiation of mouse and human BMSCs. Overexpression of miR‑483  ...[more]

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