Effect of miR-26a-5p on the Wnt/Ca(2+) Pathway and Osteogenic Differentiation of Mouse Adipose-Derived Mesenchymal Stem Cells.
Li S., Hu C., Li J., Liu L., Jing W., Tang W.
Animal Study, published in Calcif Tissue Int (2016) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Calcif Tissue Int (2016)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 27040676
- DOI
- 10.1007/s00223-016-0137-3
- Citations
- 40
Abstract (original English)
Elucidation of the molecular mechanisms that regulate the differentiation of adipose-derived mesenchymal stem cells into osteogenic cells may lead to new methods for bone tissue engineering. We examined the role of miR-26a-5p in the regulation of osteogenic differentiation of mouse adipose-derived mesenchymal stem cells (mADSCs) by using mimics and inhibitors of this microRNA. Our results showed that over-expression of miR-26a-5p inhibited osteogenesis and that suppression of endogenous miR-26a-5p promoted osteogenesis. Four bioinformatics algorithms indicated that the 3'UTR of Wnt5a was a potential target of miR-26a-5p. We confirmed this prediction by use of dual-luciferase reporter assay and GFP/RFP assay. We also examined the molecular mechanisms by which miR-26a-5p regulates osteogenesis. Fura-2AM and Western blot assays after transfection indicated that miR-26a-5p repressed WNT5A, inhibited calcium flux and protein kinase C, and suppressed osteogenic differentiation of mADSCs. By contrast, miR-26a-5p inhibition activated these signal proteins and promoted osteogenic differentiation. Taken together, our results suggest that up-regulation of miR-26a-5p inhibits osteogenic differentiation of mADSCs by directly targeting the 3'UTR of Wnt5a, thereby down-regulating the Wnt/Ca(2+) signaling pathway.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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