Acetylation of H3K18 activated by p300 promotes osteogenesis in human adipose-derived mesenchymal stem cells.
Zeng L., Chen C., Xiong Y., Liu Y., Huang M., Ye J.
Laboratory Study, published in Biochem Pharmacol (2025) — 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
- Biochem Pharmacol (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40164340
- DOI
- 10.1016/j.bcp.2025.116901
- Citations
- 1
Abstract (original English)
Human adipose-derived mesenchymal stem cells (hAD-MSCs) have garnered significant interest as a viable alternative source of stem cells for applications in bone tissue engineering due to their high and ease availability. At present, the limited studies on potential epigenetic regulatory mechanism in hAD-MSCs greatly hinders its clinical application in bone repair. Histone acetylation has been identified as a critical regulator of the osteogenic differentiation of mesenchymal stem cells (MSCs), with increased levels of histone acetylation sites frequently correlating with enhanced osteogenic differentiation. However, their specific roles in MSCs osteogenesis remain unclear. In this study, we observed a significant up-regulation of H3K18 acetylation (H3K18ac) during the osteogenic induction of hAD-MSCs. This modification was notably enriched in the promoter regions of genes associated with osteogenesis, thereby facilitating osteogenic differentiation. Furthermore, the treatment of histone acetyltransferases p300 inhibitor A-485 in hAD-MSCs resulted in a reduction of H3K18 acetylation levels during the osteogenic differentiation, which corresponded with a diminished osteoblast phenotype and function. These results indicated that p300-mediated acetylation of H3K18 enhances the osteogenic differentiation of hAD-MSCs. It provides a novel insight into understanding the mechanism of os
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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