ArticleArchives of dermatological research2025
The secretion of TGF-β3 by adipose-derived stem cells inhibits melanin synthesis and its impact on the cAMP/PKA signaling pathway.
Article in Archives of dermatological research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
This study aimed to investigate the role of transforming growth factor-beta 3 (TGF-β3) secreted by adipose-derived stem cells (ADSCs) in suppressing melanin synthesis during the wound healing process, particularly in burn injuries, and to explore the underlying mechanisms involving the cAMP/PKA signaling pathway. ADSCs were isolated from C57BL/6 mice and characterized using flow cytometry and differentiation assays. A burn injury model was established in mice, followed by UVB irradiation to induce hyperpigmentation. Mice were divided into four groups: control (PBS), ADSCs, ADSCs with TGF-β3 overexpression, and ADSCs with TGF-β3 knockdown. Melanin deposition was assessed via Fontana Masson staining, while ELISA measured the expression of MC1R and α-MSH. Western blotting was used to examine TGF-β3 and the activation of cAMP/PKA signaling pathway. Mice treated with ADSCs overexpressing TGF-β3 showed significant reductions in melanin deposition and suppressed expression of MC1R and α-MSH compared to controls. Western blot results revealed that the cAMP/PKA signaling pathway was downregulated in the TGF-β3-overexpressing ADSC group. In contrast, the knockdown of TGF-β3 led to increased melanin deposition and higher cAMP/PKA pathway activity, correlating with greater expression of MC1R and α-MSH. TGF-β3 secreted by ADSCs effectively inhibits melanin synthesis during wound healing, with potential effects on the cAMP/PKA signaling pathway. These findings suggest that TGF-β3 could serve as a potential therapeutic target for managing post-burn hyperpigmentation.
Indexed as
Identifiers
39825927What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.