LINC00173 promotes the apoptosis of hypertrophic scar fibroblasts through increasing β-catenin expression
LINC00173 promotes the apoptosis of hypertrophic scar fibroblasts through increasing β-catenin expression
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LINC00173 通过增加 β-catenin 表达促进肥厚性疤痕成纤维细胞凋亡
DOI：
10.1007/s11010-020-03966-6
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发表时间：
2020-11-03
影响因子：
4.3
通讯作者：
Li, Jun
中科院分区：
文献类型：
--
作者：
Li, Qian;Chen, Xin;Li, Jun
先前的研究已经证明了长基因间非蛋白编码RNA 173（LINC 00173）在几种病理性疾病中的参与。然而，LINC 00173在增生性瘢痕中的功能尚不清楚。本研究证实，TSV 1和TSV 2的两种转录变体在增生性瘢痕成纤维细胞中均上调。TSV 1和TSV 2的过表达可促进成纤维细胞的凋亡，而TSV 2的过表达则抑制成纤维细胞的增殖。RNA-seq、京都基因和基因组百科全书（KEGG）通路分析和基因集富集分析（GSEA）显示，磷脂酰肌醇3-激酶（PI 3 K）/Akt和丝裂原活化蛋白激酶（MAPK）信号通路可能参与LINC 00173在增生性瘢痕发病机制中的作用。此外，在TSV 1或TSV 2过表达组中，β-连环蛋白的蛋白表达上调。总体而言，该研究表明LINC 00173通过增加β-catenin表达促进成纤维细胞凋亡，表明LINC 00173可能是治疗增生性瘢痕的新靶点。
Previous studies have demonstrated the involvement of long intergenic nonprotein coding RNA 173 (LINC00173) in several pathological disorders. However, the function of LINC00173 in the hypertrophic scar is not well understood. This study confirmed that the two transcript variants of TSV1 and TSV2 were both upregulated in hypertrophic scar fibroblasts. The overexpression of TSV1 or TSV2 promoted the apoptosis of fibroblasts, whereas the overexpression of TSV2 inhibited the proliferation of fibroblasts. RNA-sequencing (RNA-seq), Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis, and gene set enrichment analysis (GSEA) showed that phosphatidylinositol 3-kinase (PI3K)/Akt and Mitogen-activated protein kinases (MAPK) signaling might be involved in the role of LINC00173 in hypertrophic scar pathogenesis. Furthermore, the protein expression of beta-catenin was upregulated in the TSV1 or TSV2 overexpression group. Overall, the study demonstrated that LINC00173 promoted the apoptosis of fibroblasts through increasing beta-catenin expression, suggesting that LINC00173 might be a new target for hypertrophic scar treatment.