Dynamic Histone Modification Patterns in Key Transcription Factor Genes During Porcine Adipogenesis
Aksoy MO., Wozniak J., Stachowiak M., Szczerbal I.
Animal Study on Hip, published in Genes (Basel) (2026) — 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
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- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Animal Study
- Journal
- Genes (Basel) (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 42194978
- PMCID
- PMC13205497
- DOI
- 10.3390/genes17050521
Abstract (original English)
Background Adipogenesis is governed by a complex interplay between transcriptional regulation and epigenetic remodeling. While many transcriptional pathways have been well characterized, less is known about how chromatin-level regulation shapes the timing of gene expression, particularly in large animal models such as pigs. In this study, we investigated histone modification patterns associated with four key adipogenic transcription factor genes- PPARG , GATA2 , CEBPA , and CEBPB -in porcine mesenchymal stem cells (MSCs) undergoing adipogenic differentiation. Methods Using RT-qPCR and ChIP-qPCR, we profiled gene transcription levels and epigenetic marks, including promoter- and exon-specific enrichment of the activating histone marks H3K9ac and H4K8ac, as well as the repressive mark H4K20me3, across six time points (day 0, 2, 4, 6, 8, and 10). Results Although PPARG and GATA2 are located in close proximity on porcine chromosome 13, they exhibited distinct histone modification profiles. PPARG showed progressive promoter acetylation (H4K8ac) accompanied by transcriptional activation, whereas GATA2 displayed decreased exon acetylation (H3K9ac) associated with declining expression. In contrast, the H4K20me3 profile was similar for both genes, suggesting no direct association with their transcriptional activity. Interestingly, CEBPA (chromosome 6) and CEBPB (chromosome 17) exhibited
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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