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• W4385663783 abstract "Abstract Purpose Mesenchymal stem cells (MSCs) can promote burn wound healing, skin appearance, and function recovery by promoting the differentiation and migration of fibroblasts of a wound. The burn environment can activate the autophagy of MSCs. However, it is not clear whether this autophagy can affect the proliferation and migration of fibroblasts. Methods In this study, pretreated MSCs with rapamycin and 3‐methyladenine modulated autophagy and co‐cultured with fibroblasts of burn. Cell migration was detected by immunofluorescence chemical staining. Western blot analysis and enzyme‐linked immunosorbent assay were performed to detect 2,3‐Dioxygenase (IDO), cytokine synthesis inhibitory factor 10 (IL‐10), cytokine synthesis inhibitory factor 6 (IL‐6), prostaglandin E2 (PGE2), transforming growth factor beta 1 (TGF‐β1) proteins levels, and the autophagy proteins p62 and microtubule‐associated protein LC3‐II/I. Results We demonstrated that autophagy regulates MSCs survival and proliferation in burn wound transplants and found that autophagy inhibition with 3‐methyladenine reduced MSCs‐mediated, fibroblast proliferation and migration in burn environment. However, rapamycin‐induced autophagy had the opposite effect and increased the TGF‐β1 expression. Therefore, we speculate that MSCs may promote fibroblast proliferation and migration by secreting TGF‐β1 via the AKT/mTOR (RAC‐alpha serine/threonine‐protein kinase/mammalian target of rapamycin) pathway. Conclusion Autophagy of MSCs regulates burn wound fibroblast proliferation and migration by affecting TGF‐β1 and prostaglandin E2 production adjacent to MSCs transplanted on the burn wound. The results of this study provide a potential strategy for promoting MSCs treatment of burns." @default.
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• W4385663783 date "2023-08-01" @default.
• W4385663783 modified "2023-09-27" @default.
• W4385663783 title "The mechanisms related to fibroblasts in burn surface" @default.
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• W4385663783 doi "https://doi.org/10.1111/srt.13431" @default.
• W4385663783 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37632175" @default.
• W4385663783 hasPublicationYear "2023" @default.
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