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KANK4 的特异性表达促进了瘢痕疙瘩组织中成纤维细胞的迁移。

Exclusive expression of KANK4 promotes myofibroblast mobility in keloid tissues.

机构信息

Department of Plastic and Reconstructive Surgery, Aichi Children's Health and Medical Center, Obu, Japan.

Department of Plastic and Reconstructive Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8560, Japan.

出版信息

Sci Rep. 2024 Apr 16;14(1):8725. doi: 10.1038/s41598-024-59293-z.

DOI:10.1038/s41598-024-59293-z
PMID:38622256
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11018845/
Abstract

Keloids are characterized by abnormal wound healing with excessive accumulation of extracellular matrix. Myofibroblasts are the primary contributor to extracellular matrix secretion, playing an essential role in the wound healing process. However, the differences between myofibroblasts involved in keloid formation and normal wound healing remain unclear. To identify the specific characteristics of keloid myofibroblasts, we initially assessed the expression levels of well-established myofibroblast markers, α-smooth muscle actin (α-SMA) and transgelin (TAGLN), in scar and keloid tissues (n = 63 and 51, respectively). Although myofibroblasts were present in significant quantities in keloids and immature scars, they were absent in mature scars. Next, we conducted RNA sequencing using myofibroblast-rich areas from keloids and immature scars to investigate the difference in RNA expression profiles among myofibroblasts. Among significantly upregulated 112 genes, KN motif and ankyrin repeat domains 4 (KANK4) was identified as a specifically upregulated gene in keloids. Immunohistochemical analysis showed that KANK4 protein was expressed in myofibroblasts in keloid tissues; however, it was not expressed in any myofibroblasts in immature scar tissues. Overexpression of KANK4 enhanced cell mobility in keloid myofibroblasts. Our results suggest that the KANK4-mediated increase in myofibroblast mobility contributes to keloid pathogenesis.

摘要

瘢痕疙瘩的特征是异常的伤口愈合,伴有细胞外基质的过度积累。肌成纤维细胞是细胞外基质分泌的主要贡献者,在伤口愈合过程中起着至关重要的作用。然而,瘢痕疙瘩形成和正常伤口愈合过程中肌成纤维细胞的差异尚不清楚。为了确定瘢痕疙瘩肌成纤维细胞的特定特征,我们首先评估了在瘢痕和瘢痕疙瘩组织中α-平滑肌肌动蛋白(α-SMA)和转胶蛋白(TAGLN)等成熟肌成纤维细胞标志物的表达水平(分别为 n=63 和 51)。尽管肌成纤维细胞在瘢痕疙瘩和未成熟瘢痕中大量存在,但在成熟瘢痕中不存在。接下来,我们使用富含肌成纤维细胞的瘢痕疙瘩和未成熟瘢痕的 RNA 测序,研究肌成纤维细胞之间的 RNA 表达谱差异。在显著上调的 112 个基因中,KN 基序和锚蛋白重复结构域 4(KANK4)被鉴定为瘢痕疙瘩中特异性上调的基因。免疫组织化学分析显示 KANK4 蛋白在瘢痕疙瘩组织中的肌成纤维细胞中表达;然而,在未成熟瘢痕组织中的任何肌成纤维细胞中均未表达。KANK4 的过表达增强了瘢痕疙瘩肌成纤维细胞的迁移能力。我们的结果表明,KANK4 介导的肌成纤维细胞迁移增加导致了瘢痕疙瘩的发病机制。

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