Ten-Eleven Translocation 1 and 2 Enzymes Affect Human Skin Fibroblasts in an Age-Related Manner
Kołodziej-Wojnar P., Borkowska J., Domaszewska-Szostek A., Bujanowska O., Noszczyk B., Krześniak N.
Laboratory Study, published in Biomedicines (2023) — 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
- Biomedicines (2023)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 37371754
- PMCID
- PMC10296407
- DOI
- 10.3390/biomedicines11061659
- Citations
- 3
Abstract (original English)
Ten-eleven translocation (TET) enzymes catalyze the oxidation of 5-methylcytosine (5mC), first to 5-hydroxymethylcytosine (5hmC), then to 5-formylcytosine (5fC), and finally to 5-carboxycytosine (5caC). Evidence suggests that changes in TET expression may impact cell function and the phenotype of aging. Proliferation, apoptosis, markers of autophagy and double-strand DNA break repair, and the expression of Fibulin 5 were assessed by flow cytometry in TET1 and TET2-overexpressing fibroblasts isolated from sun-unexposed skin of young (23-35 years) and age-advanced (75-94 years) individuals. In cells derived from young individuals, TET1 overexpression resulted in the inhibition of proliferation and apoptosis by 37% ( p = 0.03) and 24% ( p = 0.05), respectively, while the overexpression of TET2 caused a decrease in proliferation by 46% ( p = 0.01). Notably, in cells obtained from age-advanced individuals, TETs exhibited different effects. Specifically, TET1 inhibited proliferation and expression of autophagy marker Beclin 1 by 45% ( p = 0.05) and 28% ( p = 0.048), respectively, while increasing the level of γH2AX, a marker of double-strand DNA breaks necessary for initiating the repair process, by 19% ( p = 0.04). TET2 inhibited proliferation by 64% ( p = 0.053) and increased the level of γH2AX and Fibulin 5 by 46% ( p = 0.007) and 29% ( p = 0.04), respectively. These patterns of T
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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