Department of Plastic & Cosmetic Surgery, Women's Hospital of Nanjing Medical University (Nanjing Maternity and Child Health Care Hospital), 123rd Tianfei Street, Mochou Road, Nanjing, 210004, China.
Department of Caridology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China.
Mol Cell Biochem. 2021 Feb;476(2):1005-1014. doi: 10.1007/s11010-020-03966-6. Epub 2020 Nov 3.
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 β-catenin was upregulated in the TSV1 or TSV2 overexpression group. Overall, the study demonstrated that LINC00173 promoted the apoptosis of fibroblasts through increasing β-catenin expression, suggesting that LINC00173 might be a new target for hypertrophic scar treatment.
先前的研究表明,长链非编码 RNA 173(LINC00173)参与了几种病理紊乱。然而,LINC00173 在肥厚性瘢痕中的功能尚不清楚。本研究证实,TSV1 和 TSV2 的两个转录变体在肥厚性瘢痕成纤维细胞中均上调。TSV1 或 TSV2 的过表达促进了成纤维细胞的凋亡,而 TSV2 的过表达抑制了成纤维细胞的增殖。RNA 测序(RNA-seq)、京都基因与基因组百科全书(KEGG)通路分析和基因集富集分析(GSEA)表明,磷脂酰肌醇 3-激酶(PI3K)/Akt 和丝裂原活化蛋白激酶(MAPK)信号通路可能参与了 LINC00173 在肥厚性瘢痕发病机制中的作用。此外,在 TSV1 或 TSV2 过表达组中β-连环蛋白的蛋白表达上调。总的来说,该研究表明 LINC00173 通过增加β-连环蛋白的表达促进成纤维细胞凋亡,提示 LINC00173 可能是肥厚性瘢痕治疗的一个新靶点。