TRIB3 Promotes Osteogenic Differentiation of Human Adipose-derived Mesenchymal Stem Cells Levelled by Post-transcriptional Regulation of miR-24-3p.
Bai XS., Zhang P., Liu YS., Liu H., Lv LW., Zhou YS.
Laboratory Study, published in Chin J Dent Res (2021) — 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
- Chin J Dent Res (2021)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 35029095
- DOI
- 10.3290/j.cjdr.b2440815
- Citations
- 6
Abstract (original English)
Objective To explore the effect of TRIB3 on the osteogenic differentiation of human adipose-derived mesenchymal stem cells (hASCs) and reveal the potential role of TRIB3 in bone regeneration. Methods TRIB3-knockdown and TRIB3-overexpression hASCs were used to explore the effect of TRIB3 on osteogenic differentiation by alkaline phosphatase (ALP) staining, alizarin red S (ARS) staining, quantitative real-time polymerase chain reaction (qRT-PCR) and heterotopic bone formation. The regulation of miR-24-3p on TRIB3 was detected by qRT-PCR and western blot. Ribonucleic acid (RNA) sequencing was performed to investigate the downstream regulatory network of TRIB3. Results TRIB3 promoted the osteogenic differentiation of hASCs both in vitro and in vivo. This process was regulated epigenetically by the post-transcriptional regulation of miR-24-3p, which could bind directly to the three prime untranslated region (3'UTR) of TRIB3 and inhibit TRIB3 expression. The downstream regulatory network of TRIB3-mediated osteogenic differentiation was related to calcium ion binding and cell metabolism, extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and nuclear factor-κB (NF-κB) signalling pathways. Conclusion TRIB3 is a promising therapeutic target for hASC-based bone tissue engineering and the epigenetic regulation of TRIB3 through miR-24-3p permits regulatory controllability, thus
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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