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Single-cell RNA-seq reveals immune cell heterogeneity and increased Th17 cells in keloid

ABSTRACT: The immune response is postulated to exert a pivotal role in the occurrence and progression of keloid. In recent years, the impact of the peripheral immune microenvironment on keloid has garnered significant attention in scholarly investigations exploring the underlying pathogenesis of this condition. In this study, we isolated CD45+ cells from keloid and normal scar dermis tissues by fluorescence activated cell sorting (FACS) and performed single-cell RNA sequencing analysis. Our results revealed the intricate cellular landscape of immune cells in keloid. We found that compared to normal scar tissue, the percentage of Th17 cells was significantly increased in keloid. Further functional studies revealed that Th17 cell promotes proliferation, migration and collagen expression of keloid fibroblast through IL17a. These findings will help us more thoroughly understand keloid pathogenesis and provide potential targets for keloid therapies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE270438 | GEO | 2025/01/06

REPOSITORIES: GEO

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Keloid-specific gene expression profiling for accurate diagnostic and therapeutic applications.

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Keloid fibroproliferative properties are dependent on stem cells modified by the HEDGEHOG-GLI1 pathway [EA1874]

2023-12-13 | GSE218894 | GEO

WNT5A Drives IL-6-Dependent Epithelial-to-Mesenchymal Transition via the JAK/STAT Pathway in Keloid Pathogenesis

Project description:Purpose: We aimed to identify the molecular drivers that initiate or sustain keloid pathogenesis. Method: Bulk tissue RNA sequencing of Asian keloid and normal tissues was performed to identify genes that contribute to keloid pathogenesis. We also established a preclinical model of inflammatory skin fibrosis by injecting C57BL/6 mice with bleomycin intradermally for 3 weeks to provide an alternative animal model of keloid scar. Result: Gene set enrichment analysis revealed upregulation of WNT5A gene expression, along with significant enrichment of genes related to EMT in keloid tissues. These results correlate with those of histological analysis in which human keloid tissues and the bleomycin-induced fibrosis animal model showed increased WNT5A expression along with EMT markers. Our in vitro data showed increased expression of the IL-6/JAK/STAT pathway and subsequent elevation in EMT markers on keratinocytes when co-cultured with WNT5A-activated fibroblasts or keloid fibroblasts. Silencing of WNT5A reversed the hyperactivation of the STAT pathway and EMT. Conclusion: IL-6 secreted from WNT5A-activated fibroblasts or keloid fibroblasts may induce adjacent keratinocytes to express EMT markers by activating the JAK/STAT signalling pathway. A better understanding of keloid pathogenesis and the role of WNT5A in EMT will promote the development of next-generation targeted treatments for keloid scars.

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Project description:This study investigated the effects of extracellular matrix (ECM) rigidty on gene expression patterns in normal dermal fibroblasts (NDFs) and keloid dermal fibroblasts (KDFs). Cells were cultured on collagen coated polyacrylamide hydrogels with elastic moduli mimicking normal skin (8 kPa) or keloid scar tissue (214 kPa), and changes in gene expression were profiled using next-generation RNA-sequencing. Differential gene expression analysis identified overall significant differences in gene expression between the NDF and KDF populations. Despite high levels of inter-patient heterogeneity in the KDF samples, further principal components analysis revealed a subset of genes (PC5) that were specifically regulated by ECM rigidity. Gene set enrichment analysis of the PC5 genes identified classic pathways associated with mechanotransduction, including Hippo Signalling and Regulation of the Actin Cytoskeleton, as well as genes associated with the Autophagy pathway. Additional in vitro studies and human tissue staining confirmed the biomechanical regulation of autophagic flux in NDFs and KDFs and differential remodelling of the lysosome in KDFs and keloid scars. Together, these findings implicate autophagy and lysosomal remodelling as biomechanically dysregulated pathways in keloid fibroblasts, and these mechanisms may contribute to scar pathogenesis.

2023-11-02 | GSE246562 | GEO

The Role of the Mammalian Target of Rapamycin in Keloid and Hypertrophic Scars

Project description:We hypothesize that, the mTOR pathway is a dominant pathway in cultured keloid and hypertrophy scar fibriblasts compared to normal skin cells. Certain pathway changes can be detected after medication treatment. Global gene expression in RNA samples from rapamycin and tacrolimus treated fibroblasts (from normal skin and hypertrophic scars, keloid scars) is assayed to study the possibility to use mTOR inhibitors as potential drug to treat abnormal scarring. We investigated the difference between normal wound healing and hypertrophic scars and keloids as well.

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