Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Distinct diversity of skin cell populations of rhinophyma and hypertrophic scar illustrated by scRNA-seq

ABSTRACT: The clinical manifestations and presentation of rhinophyma closely resemble those of hypertrophic scar tissue, both presenting as firm, fibrotic growths. Despite this phenotypic similarity, a critical divergence is observed following surgical intervention: the affected skin in rhinophyma can revert to its normal state without scar recurrence, a favorable outcome starkly contrasting with the behavior of hypertrophic scars. The underlying mechanisms for this phenomenon have yet to be elucidated. The aim of this study is to uncover the cellular and molecular disparities between these two pathological conditions using single-cell sequencing technology to resolve this clinical paradox. The objective of this study is to compare the single-cell transcriptomic profiles of rhinophyma and hypertrophic scar tissues to identify key cell types and molecular pathways that may account for the distinct healing fate of rhinophyma post-surgery and provide novel insights for the prevention and treatment of hypertrophic scars.

INSTRUMENT(S): 10X Genomics Chromium Controller Instrument, Thermocycler (PCR machine), Bioanalyzer 2200 (Agilent), Qubit Fluorometer (Thermo Fisher Scientific), Surgical scalpel, Biological safety cabinet, Water bath (37°C), Centrifuge, 70 µm and 35 µm cell strainers, Countstar Fluorescence Cell Analyzer, Illumina NovaSeq 6000

ORGANISM(S): Homo sapiens

SUBMITTER: Lanxin Geng

PROVIDER: E-MTAB-16629 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Hypertrophic scars, which result from aberrant fibrosis and disorganized collagen synthesis by skin fibroblasts, emerge due to disrupted wound healing processes. These scars present significant psychosocial and functional challenges to affected individuals. The current treatment limitations largely arise from an incomplete understanding of the underlying mechanisms of hypertrophic scar development. Recent studies, however, have shed light on the potential of exosomal non-coding RNAs interventions to mitigate hypertrophic scar proliferation. This research assesses the impact of exosomes derived from adipose-derived stem cells (ADSCs-Exos) on hypertrophic scar formation using a rabbit ear model. We employed Hematoxylin and Eosin staining, Masson’s Trichrome staining, and Immunohistochemical staining techniques to track scar progression. Our comprehensive analysis encompassed the differential expression of non-coding RNAs, enrichment analyses of functional pathways, protein-protein interaction studies, and miRNA-mRNA interaction investigations. The results reveal a marked alteration in the expression levels of long non-coding RNAs and microRNAs following ADSCs-Exos treatment, with little changes observed in circular RNAs. Notably, miR-194 emerges as a critical regulator within the signaling pathways that govern hypertrophic scar formation. Dual-luciferase assays indicated a significant reduction in the promoter activity of TGF-β1 after miR-194 overexpression. Quantitative reverse transcription PCR and Western blotting assays further validated the decrease in TGF-β1 expression in the treated samples. Moreover, the treatment resulted in diminished levels of inflammatory markers IL-1β, TNF-α, and IL-10. In vivo evidence strongly supports the role of miR-194 in attenuating hypertrophic scar formation through the suppression of TGF-β1. Our findings endorse the strategic use of ADSCs-Exos, particularly through miR-194 modulation, as an effective strategy for reducing scar formation and lowering pro-inflammatory and fibrotic indicators like TGF-β1. Therefore, this study advocates for the targeted application of ADSCs-Exos, with an emphasis on miR-194 modulation, as a promising approach to managing proliferative scarring.

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Distinct diversity of skin cell populations of rhinophyma and hypertrophic scar illustrated by scRNA-seq

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