MiR-122-3p regulates the osteogenic differentiation of mouse adipose-derived stem cells via Wnt/β catenin signaling pathway.
Hao W., Liu HZ., Zhou LG., Sun YJ., Su H., Ni JQ.
Animal Study, published in Eur Rev Med Pharmacol Sci (2019) — 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
- Eur Rev Med Pharmacol Sci (2019)
- Country
- Italy
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 31115017
- DOI
- 10.26355/eurrev_201905_17817
- Citations
- 2
Abstract (original English)
Objective To explore the regulatory mechanism of micro-ribonucleic acid (miR)-122-3p in the osteogenic differentiation of mouse adipose-derived stem cells (mADSCs). Materials and methods The regulatory mechanism of miR-122-3p in the osteogenic differentiation of mesenchymal stem cells was investigated through its overexpression and knockdown. Results The overexpression of miR-122-3p inhibited the osteogenic differentiation of mADSCs. On the contrary, its knockdown promoted the osteogenic differentiation of mADSCs. The further study on the molecular mechanism of miR-122-3p regulating mADSCs' osteogenic differentiation showed that the overexpression of miR-122-3p could activate the Wingless and int-1 (WNT)/β-catenin signaling pathway, but the knockdown of miR-122-3p could repress this signaling pathway. Conclusions MiR-122-3p influences the osteogenic differentiation of mADSCs by modulating the WNT/β-catenin 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.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.