MiR-125a-3p negatively regulates osteoblastic differentiation of human adipose derived mesenchymal stem cells by targeting Smad4 and Jak1.
Gu Z., Long J., Li Y., Wang X., Wang H.
Laboratory Study, published in Am J Transl Res (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
- Laboratory Study
- Journal
- Am J Transl Res (2019)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 31105866
- PMCID
- PMC6511781
- Citations
- 13
Abstract (original English)
Osteogenesis is a complex process which relies on the coordination of signals and transcription factors. Recent evidence indicates that microRNAs (miRNAs) act as important post-transcriptional regulators in a large number of biological processes including osteoblast differentiation. In this study, we investigated the expression and biological effect of miR-125a-3p during osteogenic differentiation of human adipose derived mesenchymal stem cells (hADSCs). We observed an obvious decrease in miR-125a-3p level during osteogenic differentiation. By using gain- and loss-of function experiments, we noticed that miR-125a-3p could suppress the osteogenic differentiation of hADSCs. Moreover, miR-125a-3p over-expression in hADSCs by transfection with miR-125a-3p mimics significantly inhibited cell proliferation by MTT. Flow cytometry analysis further demonstrated that forced expression of miR-125a-3p induced cell cycle G 1 /S phase arrest and apoptosis. In addition, we performed bioinformatic analysis, luciferase reporter assay and western blot to confirm that miR-125a-3p could regulate Smad4 and Jak1 expression negatively. Meanwhile, Smad4 and Jak1 were up-regulated after osteogenic differentiation and the down-regulation of endogenous Smad4 and Jak1 suppressed the osteogenic differentiation of hADSCs. Taken together, these data indicated that miR-125a-3p is Smad4 and Jak1 regulator, and
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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