Abstract
BackgroundThe pathophysiology of keloid formation is not yet understood, so the identification of biomarkers for kelod can be one step towards designing new targeting therapies which will improve outcomes for patients with keloids or at risk of developing keloids.MethodsIn this study, we performed single-cell RNA sequencing analysis, weighted co-expression network analysis, and differential expression analysis of keloids based on public databases. And 3 RNA sequencing data from keloid patients in our center were used for validation. Besides, we performed QRT-PCR on keloid tissue and adjacent normal tissues from 16 patients for further verification.ResultsWe identified the sensitive biomarker of keloid: Tenascin-C (TNC). Then, Pseudotime analysis found that the expression level of TNC decreased first, then stabilized and finally increased with fibroblast differentiation, suggesting that TNC may play an potential role in fibroblast differentiation. In addition, there were differences in the infiltration level of macrophages M0 between the TNC-high group and the TNC-low group. Macrophages M0 had a higher infiltration level in low TNC- group (P<0.05).ConclusionOur results can provide a new idea for the diagnosis and treatment of keloid.
Highlights
Wound healing plays an important role in maintaining skin barrier function (1)
Keloid and the surrounding 1cm of normal tissue were resected by the same surgeon
After the differential genes were sorted down according to logFC, Gene Set Enrichment Analysis (GSEA) analysis was performed, and the result of P
Summary
Wound healing plays an important role in maintaining skin barrier function (1). The final form of the wound is a scar (2). Its clinical manifestation is scar hyperplasia beyond the wound, invasive growth (4). It does not TNC, Biomarker for Keloid gradually fade, often accompanied by pain and itching discomfort (4). Exploring the pathogenesis of keloid is helpful to promote the development of new treatment regimens. Exploring changes in the immune microenvironment of keloid can deepen our understanding of the pathogenesis of keloid, and promote the treatment of keloid patients to improve the prognosis. The pathophysiology of keloid formation is not yet understood, so the identification of biomarkers for kelod can be one step towards designing new targeting therapies which will improve outcomes for patients with keloids or at risk of developing keloids
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