Dose-dependent biphasic effect of environmental UVA on stem cell function through PRPF40A, TGF-β1, NFATc1 signaling.
Zheng Q., Ngo HTT., Nguyen TTM., Kim JW., Choi JW., Yi TH.
Laboratory Study on Face & Skin, Hair & Scalp, Hip, published in J Photochem Photobiol B (2026) — summary generated from the PubMed abstract.
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
- J Photochem Photobiol B (2026)
- Country
- Switzerland
- Reported sample size
- —
- PMID
- 41950867
- DOI
- 10.1016/j.jphotobiol.2026.113435
Abstract (original English)
Solar ultraviolet A (UVA) radiation makes up nearly 95% of the ultraviolet spectrum at the Earth's surface, forming a major environmental exposure. High-dose UVA is a well-established driver of phototoxicity and tissue degeneration; however, the impact of low-dose UVA on stem-cell homeostasis remains incompletely defined. Here, we investigated whether UVA elicits a dose-dependent biphasic response in human adipose-derived mesenchymal stem cells (AMSCs) and evaluated PRPF40A as a molecular indicator of stemness status. AMSCs were exposed to single or fractionated UVA regimens (0.05-2 J/cm 2 ), followed by assessments of viability, migration, oxidative stress, apoptosis and senescence, stemness programs, multilineage differentiation, and secretome remodeling. In cultured human AMSCs, UVA induced a biphasic dose-response pattern. An ultra-low dose (0.05 J/cm 2 ) enhanced viability and migratory capacity, reduced basal reactive oxygen species, preserved NANOG/SOX2/OCT4 expression, and promoted chondrogenic potential. In contrast, doses of 0.5 J/cm 2 or higher, particularly under cumulative exposure, induced oxidative injury, apoptosis, senescence-like changes, reduced stemness, impaired differentiation, and a pro-inflammatory senescence-associated secretory phenotype. Mechanistically, PRPF40A was inversely associated with stemness and showed dose-dependent co-regulation with TGF-β1
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 comes from animal or laboratory studies and has not been confirmed in humans.
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