瘢痕疙瘩（KL）是一种常见的良性皮肤肿瘤。 KL 的典型特征是显着的纤维化和强烈的炎症反应。因此，全面了解细胞炎症和纤维化细胞之间的相互作用对于阐明驱动 KL 进展的机制和开发治疗方法至关重要。研究瘢痕疙瘩中炎症和纤维化的转录组图谱。在本文中，我们进行了转录组测序对来自六种人类瘢痕疙瘩组织和正常皮肤组织的未选择的活细胞进行 microRNA (miRNA) 测序，以阐明全面的转录组图谱。此外，我们使用单细胞 RNA 测序 (scRNA-seq) 分析来分析细胞间通讯网络，并富集另外两个疤痕疙瘩和正常皮肤样本中的成纤维细胞群体，以研究成纤维细胞多样性。通过 RNA 测序和 miRNA-mRNA-PPI 网络分析，我们确定 miR-615-5p 和 miR-122b-3p 可能是与疤痕疙瘩相关的 miRNA，因为它们在疤痕疙瘩中差异最为显着。同样，COL3A1、COL1A2、THBS2、TNC、IGTA、THBS4、TGFB3作为与疤痕疙瘩差异显着的基因，可能与疤痕疙瘩的发生有关。使用从正常或瘢痕疙瘩收集的 24,086 个细胞的单细胞 RNA 测序数据，我们报告了重建的细胞间信号网络分析和聚合到细胞水平上与特定细胞亚群相关的模块以进行瘢痕疙瘩改变。我们的多转录组数据集描绘了人类的炎症和纤维异质性疤痕疙瘩，强调炎症细胞和纤维细胞之间细胞间串扰的重要性，并揭示潜在的治疗靶点。版权所有 © 2024 日本皮肤病研究学会。由 Elsevier B.V. 出版。保留所有权利。

Keloid (KL) is a common benign skin tumor. KL is typically characterized by significant fibrosis and an intensive inflammatory response. Therefore, a comprehensive understanding of the interactions between cellular inflammation and fibrotic cells is essential to elucidate the mechanisms driving the progression of KL and to develop therapeutics.Investigate the transcriptome landscape of inflammation and fibrosis in keloid scars.In this paper, we performed transcriptome sequencing and microRNA (miRNA) sequencing on unselected live cells from six human keloid tissues and normal skin tissues to elucidate a comprehensive transcriptome landscape. In addition, we used single-cell RNA sequencing (scRNA-seq) analysis to analyze intercellular communication networks and enrich fibroblast populations in two additional keloid and normal skin samples to study fibroblast diversity.By RNA sequencing and a miRNA-mRNA-PPI network analysis, we identified miR-615-5p and miR-122b-3p as possible miRNAs associated with keloids, as they differed most significantly in keloids. Similarly, COL3A1, COL1A2, THBS2, TNC, IGTA, THBS4, TGFB3 as genes with significant differences in keloid may be associated with keloid development. Using single-cell RNA sequencing data from 24,086 cells collected from normal or keloid, we report reconstructed intercellular signaling network analysis and aggregation to modules associated with specific cell subpopulations at the cellular level for keloid alterations.Our multitranscriptomic dataset delineates inflammatory and fibro heterogeneity of human keloids, underlining the importance of intercellular crosstalk between inflammatory cells and fibro cells and revealing potential therapeutic targets.Copyright © 2024 Japanese Society for Investigative Dermatology. Published by Elsevier B.V. All rights reserved.