Ablation of KDM2A Inhibits Preadipocyte Proliferation and Promotes Adipogenic Differentiation
Hua Y., Yue Y., Zhao D., Ma Y., Xiong Y., Xiong X.
Animal Study, published in Int J Mol Sci (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
- Animal Study
- Journal
- Int J Mol Sci (2021)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 34575926
- PMCID
- PMC8467897
- DOI
- 10.3390/ijms22189759
- Citations
- 8
Abstract (original English)
Epigenetic signals and chromatin-modifying proteins play critical roles in adipogenesis, which determines the risk of obesity and which has recently attracted increasing interest. Histone demethylase 2A (KDM2A) is an important component of histone demethylase; however, its direct effect on fat deposition remains unclear. Here, a KDM2A loss of function was performed using two unbiased methods, small interfering RNA (siRNA) and Cre-Loxp recombinase systems, to reveal its function in adipogenesis. The results show that the knockdown of KDM2A by siRNAs inhibited the proliferation capacity of 3T3-L1 preadipocytes. Furthermore, the promotion of preadipocyte differentiation was observed in siRNA-treated cells, manifested by the increasing content of lipid droplets and the expression level of adipogenic-related genes. Consistently, the genetic deletion of KDM2A by Adipoq-Cre in primary adipocytes exhibited similar phenotypes to those of 3T3-L1 preadipocytes. Interestingly, the knockdown of KDM2A upregulates the expression level of Transportin 1(TNPO1), which in turn may induce the nuclear translocation of PPARγ and the accumulation of lipid droplets. In conclusion, the ablation of KDM2A inhibits preadipocyte proliferation and promotes its adipogenic differentiation. This work provides direct evidence of the exact role of KDM2A in fat deposition and provides theoretical support for obes
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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