ArticleJournal of cosmetic dermatology2024
Hepatocyte growth factor-modified adipose-derived mesenchymal stem cells inhibit human hypertrophic scar fibroblast activation.
Article in Journal of cosmetic dermatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- LLLT-ADSCs Curtail the Progression of Keloid Through Exosomal miR-26a-5p Downregulating Jag/Notch Pathway.Lasers in surgery and medicine · 2026Article
- Adipose Stem Cell-Derived Apoptotic Vesicles Attenuate Hypertrophic Scarring by Targeting the CDC20/WNT Signaling Pathway.Biomedicines · 2026Article
- Exosome-Loaded GelMA Hydrogel as a Cell-Free Therapeutic Strategy for Hypertrophic Scar Inhibition.Clinical, cosmetic and investigational dermatology · 2025Article
- Cell-free adipose extract inhibits hypertrophic scar formation through collagen remodeling and antiangiogenesis.Open medicine (Warsaw, Poland) · 2025Article
- Hepatocyte growth factor-modified adipose-derived mesenchymal stem cells inhibit human hypertrophic scar fibroblast activation.Journal of cosmetic dermatology · 2024Article
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Abstract
purposeNucleoside-modified messenger RNA (modRNA) holds the potential for facilitating genetic enhancement of stem cells. In this study, modRNA encoding hepatocyte growth factor (modHGF) was used to chemically modify adipose-derived mesenchymal stem cells (ADSCs) and the effect of modified ADSCs on the activation of hypertrophic scar fibroblasts (HSFs) was evaluated.
methodsCCK-8, wound healing, and transwell assays were utilized to evaluate the viability and migratory potential of modHGF-engineered ADSCs and their effect on HSF activation. Reverse transcription-polymerase chain reaction, western blot, and immunofluorescence staining were performed to detect the expression of collagen-I (Col I), collagen-III (Col III), alpha-smooth muscle actin (α-SMA), matrix metallopeptidase 1 (MMP-1), and MMP-3.
resultsTransfection of ADSCs with modHGF (HGF-ADSC) resulted in enhanced production of HGF. Meanwhile, modHGF modification enhanced the viability and migration of ADSCs. Notably, culture media from HGF-ADSCs exhibited a more potent inhibitory effect on the proliferation and migration of HSFs. In addition, culture media from HGF-ADSCs inhibited extracellular matrix synthesis of HSFs, as evidenced by reduced expression levels of Col I, Col III, and α-SMA, while increasing expression of MMP-1 and MMP-3. Conversely, neutralization experiments confirmed that these effects could be effectively alleviated by blocking HGF activity.
conclusionmodHGF modification optimizes the inhibitory effect of ADSCs on HSF activation, which provides a promising alternative for preventing and treating hyperplastic scars.
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