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Epidermal stem cell-derived EVs induced myofibroblasts mesenchymal-epidermal transition alleviate scarring via the miR-200s/ZEBs axis

ABSTRACT: Epidermal stem cell-derived EVs induced myofibroblasts mesenchymal-epidermal transition alleviate scarring via the miR-200s/ZEBs axis

PROVIDER: PRJNA1214878 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32104400.fastq.gz	Fastqsanger.gz
	SRR32104401.fastq.gz	Fastqsanger.gz
	SRR32104402.fastq.gz	Fastqsanger.gz
	SRR32104403.fastq.gz	Fastqsanger.gz
	SRR32104404.fastq.gz	Fastqsanger.gz

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Epidermal stem cell-derived EVs induced myofibroblasts mesenchymal-epidermal transition alleviate scarring via the miR-200s/ZEBs axis

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Human Scarring Project

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RNA-sequencing demonstrates transcriptional differences between human vocal fold fibroblasts and myofibroblasts

Project description:Background: Differentiation of fibroblasts into myofibroblasts is necessary for wound healing, but excessive myofibroblast presence and persistence can result in scarring. Treatment for scarring is limited largely due to a lack of comprehensive understanding of how fibroblasts and myofibroblasts differ at the transcript level. The purpose of the study was to comprehensively characterize transcriptional profiles of injured fibroblasts relative to normal fibroblasts, utilizing fibroblasts from the vocal fold as a model for other areas of the body. Results: we identified differentially expressed genes between groups of normal fibroblasts, scarred fibroblasts, and fibroblasts treated with transforming growth factor-beta 1 (TGF-β1), which represented an induced-scar phenotype. Principal component analysis revealed clustering of normal fibroblasts separate from the clustering of fibroblasts treated with TGF-β1; scarred fibroblasts were more similar to normal fibroblasts than fibroblasts treated with TGF-β1. Enrichment analyses revealed pathways related to cell signaling, receptor-ligand activity, and regulation of cell functions in scarred fibroblasts, pathways related to cell adhesion in normal fibroblasts, and pathways related to ECM binding in fibroblasts treated with TGF-β1. Although transcriptomic profiles between scarred fibroblasts and fibroblasts treated with TGF-β1 were relatively dissimilar, the most highly co-expressed genes were enriched in pathways related to actin cytoskeleton binding. Conclusions: Transcriptomics of normal fibroblasts differ from myofibroblasts, including from those retrieved from scar and those treated with TGF-β1. Despite large differences in transcriptomics between tVFF and sVFF, tVFF serve as a useful in vitro model of myofibroblasts and highlight key similarities to myofibroblasts extracted from scar pathology, as well as expected differences related to normal fibroblasts from healthy VF.

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JUN promotes hypertrophic skin scarring via CD36

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Secretomes of Cancer-Associated Myofibroblasts and Normal Tissue Myofibroblasts in hypoxia and normoxia C4PR_LIV

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2019-03-04 | PXD008104 | Pride

Epidermal stem cell derived exosomes-induced dedifferentiation of myofibroblasts inhibits scarring via the miR-203a-3p/PIK3CA axis.

Project description:Hypertrophic scar (HS) is a common fibroproliferative disorders with no fully effective treatments. The conversion of fibroblasts to myofibroblasts is known to play a critical role in HS formation, making it essential to identify molecules that promote myofibroblast dedifferentiation and to elucidate their underlying mechanisms. In this study, we used comparative transcriptomics and single-cell sequencing to identify key molecules and pathways that mediate fibrosis and myofibroblast transdifferentiation. Epidermal stem cell-derived extracellular vesicles (EpiSC-EVs) were isolated via ultracentrifugation and filtration, followed by miRNA sequencing to identify miRNAs targeting key molecules. After in vitro and in vivo treatment with EpiSC-EVs, we assessed antifibrotic effects through scratch assays, collagen contraction assays, Western blotting, and immunofluorescence. Transcriptomic sequencing and rescue experiments were used to investigate the molecular mechanism by which miR-203a-3p in EpiSC-EVs induces myofibroblast dedifferentiation. Our results indicate that PIK3CA is overexpressed in HS tissues and positively correlates with fibrosis. EpiSC-EVs were absorbed by scar-derived fibroblasts, promoting dedifferentiation from myofibroblasts to quiescent fibroblasts. Mechanistically, miR-203a-3p in EpiSC-EVs plays an essential role in inhibiting PIK3CA expression and PI3K/AKT/mTOR pathway hyperactivation, thereby reducing scar formation. In vivo studies confirmed that EpiSC-EVs attenuate excessive scarring through the miR-203a-3p/PIK3CA axis, suggesting EpiSC-EVs as a promising therapeutic approach for HS.

| S-EPMC11776291 | biostudies-literature

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