Li Mingming, Wu Lei
Department of Cosmetology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, Henan 471000, P.R. China.
Department of Plastic Surgery, The No. 1 People's Hospital of Zhengzhou, Zhengzhou, Henan 450003, P.R. China.
Exp Ther Med. 2016 Dec;12(6):3633-3641. doi: 10.3892/etm.2016.3817. Epub 2016 Oct 18.
The aim of the present study was to select key genes that are associated with fibroblasts and keratinocytes during keloid scar progression and development. The gene expression profile of GSE44270, which includes 32 samples, was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) in case samples compared with control samples were screened using the Limma R package followed by hierarchical clustering analysis. Protein-protein interaction (PPI) networks of the total selected DEGs were constructed using Cytoscape. Moreover, the Gene Ontology biological processes and significant Kyoto Encyclopedia of Genes and Genomes pathways of the total selected DEGs were enriched using the Database for Annotation, Visualization and Integrated Discovery. Significant pathways that may be associated with keloid scar were analyzed using deviation analysis of dynamic capabilities. There were 658 DEGs in fibroblast keloid vs. normal, 112 DEGs in fibroblast non-lesion vs. normal, 439 DEGs in fibroblast keloid vs. non-lesion, 523 DEGs in keratocyte keloid vs. normal, 186 DEGs in keratocyte non-lesion vs. normal, and 963 DEGs in keratocyte keloid vs. non-lesion groups. HOXA9, BMP4, CDKN1A and SMAD2 in fibroblasts, and HOXA7, MCM8, PSMA4 and PSMB2 in keratinocytes were key genes in the PPI networks. Moreover, the amino sugar and nucleotide sugar metabolism pathway, cell cycle, and extracellular matrix (ECM)-receptor interaction pathway were significant pathways. This study suggests that several key genes (BMP4, HOXA9, SMAD2, CDKN1A, HOXA7, PSMA4 and PSMB2) that participate in some significant pathways (cell cycle and ECM-receptor interaction pathways) may be potential therapeutic targets for keloid scars.
本研究的目的是筛选在瘢痕疙瘩进展和发展过程中与成纤维细胞和角质形成细胞相关的关键基因。从基因表达综合数据库下载了包含32个样本的GSE44270基因表达谱。使用Limma R包筛选病例样本与对照样本中的差异表达基因(DEG),随后进行层次聚类分析。使用Cytoscape构建所有选定DEG的蛋白质-蛋白质相互作用(PPI)网络。此外,使用注释、可视化和综合发现数据库对所有选定DEG的基因本体生物学过程和京都基因与基因组百科全书重要途径进行富集。使用动态能力偏差分析来分析可能与瘢痕疙瘩相关的重要途径。在成纤维细胞瘢痕疙瘩与正常组中有658个DEG,成纤维细胞非病变与正常组中有112个DEG,成纤维细胞瘢痕疙瘩与非病变组中有439个DEG,角质形成细胞瘢痕疙瘩与正常组中有523个DEG,角质形成细胞非病变与正常组中有186个DEG,角质形成细胞瘢痕疙瘩与非病变组中有963个DEG。成纤维细胞中的HOXA9、BMP4、CDKN1A和SMAD2以及角质形成细胞中的HOXA7、MCM8、PSMA4和PSMB2是PPI网络中的关键基因。此外,氨基糖和核苷酸糖代谢途径、细胞周期以及细胞外基质(ECM)-受体相互作用途径是重要途径。本研究表明,参与某些重要途径(细胞周期和ECM-受体相互作用途径)的几个关键基因(BMP4、HOXA9、SMAD2、CDKN1A、HOXA7、PSMA4和PSMB2)可能是瘢痕疙瘩的潜在治疗靶点。