NDLI: The inhibition of MicroRNA-139-5p promoted osteoporosis of bone marrow-derived mesenchymal stem cell by targeting Wnt/beta-catenin signaling pathway by NOTCH1.

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The inhibition of MicroRNA-139-5p promoted osteoporosis of bone marrow-derived mesenchymal stem cell by targeting Wnt/beta-catenin signaling pathway by NOTCH1.

Content Provider	Semantic Scholar
Author	Feng, Yimiao Wan, Pengbo Yin, Lin-Ling Lou, Xintian
Copyright Year	2019
Abstract	To investigate the therapeutic effects of microRNA-139-5p promotes osteoporosis of bone marrow-derived mesenchymal stem cell (BMSCs) and its underlying mechanisms. This study used a dexamethasone-induced model of osteoporosis for vivo model and BMSCs was used for vitro model. Real-time quantitative polymerase chain reaction (RT-PCR) and gene chip were used to analyze the expression of microRNA-139-5p. In osteoporosis rat model, the expression of microRNA-139-5p was increased, compared with normal group. Down-regulation of microRNA-139-5p promotes cell proliferation and osteogenic differentiation in BMSCs. Especially, up-regulation of microRNA-139-5p reduced cell proliferation and osteogenic differentiation in BMSCs. Overexpression of miR-139-5p induced Wnt/β-catenin and down-regulated NOTCH1 signaling in BMSCs. Down-regulation of miR-139-5p suppressed Wnt/β-catenin and induced NOTCH1 signaling in BMSCs. The inhibition of NOTCH1 reduced the effects of anti-miR-139-5p on cell proliferation and osteogenic differentiation in BMSCs. Activation of Wnt/β-catenin also inhibited the effects of anti-miR-139-5p on cell proliferation and osteogenic differentiation in BMSCs. Taken together, our results suggested that the inhibition of microRNA-139-5p promotes osteogenic differentiation of BMSCs via targeting Wnt/beta-catenin signaling pathway by NOTCH1.
File Format	PDF HTM / HTML
DOI	10.4014/jmb.1908.08036
PubMed reference number	31752063
Journal	Medline
Journal	Journal of microbiology and biotechnology
Alternate Webpage(s)	http://www.jmb.or.kr/journal/download.php?Filedir=../submission/Journal/030/&num=10304
Alternate Webpage(s)	http://www.jmb.or.kr/journal/download.php?Filedir=../submission/Journal/029/&num=10284
Alternate Webpage(s)	https://doi.org/10.4014/jmb.1908.08036
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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