摘要
目的比较瘢痕疙瘩与正常皮肤的基因表达差异,从分子水平探讨瘢痕疙瘩的发病机制,为临床治疗提供新思路。方法用PubMed数据库文献检索瘢痕疙瘩与正常皮肤的差异表达基因,对与瘢痕疙瘩相关的基因进行蛋白-蛋白相互作用网络、生物学通路、基因本体(gene ontology,GO)和功能注释聚类的生物信息学分析。结果获得差异表达基因谱8个和文献922篇,筛选瘢痕疙瘩相关基因94个(71个上调,23个下调)。86个基因构成蛋白-蛋白相互作用网络,TGFB1、FN1、COL1A1、MMP9、VEGFA、TP53、IL6和MMP2为核心蛋白。瘢痕疙瘩相关基因参与信号转导、肿瘤形成等生物学通路,细胞凋亡、细胞运动等生物过程,形成细胞膜结构和细胞外基质、胶原等组分。结论 TGFB1、FN1、COL1A1、MMP9、VEGFA、TP53、IL6和MMP2等关键基因,TGF-β信号转导、细胞增殖和凋亡、肿瘤形成相关通路在瘢痕疙瘩的发生发展中可能起重要作用。
Objective To explore the pathogenesis of keloid by comparing the gene expression in keloid and normal skin tissues,so that to seek new therapeutic approaches for keloid. Methods The differentially expressed genes between keloid and normal skin were obtained by mining PubMed. The dysregulated genes in keloid were analyzed by bioinformatics methods, including protein-protein interaction networks, biological pathways, gene ontology and functional annotation clustering analysis. Results Eight differential gene expression datasets and 922 articles were obtained. A total of 94 dysregulated genes in keloid were identified （71 up-regulated genes and 23 down-regulated genes）. Eighty-six genes were found to encode proteins with interaction network, including TGFB1, FN1, COL1A1, MMP9, VEGFA, TP53, IL6 and MMP2 as the central nodes for this network, The dysregulated genes in keloid were involved in a variety of biological pathways, including signal transduction and tumor formation. Furthermore, the dysregulated genes in keloid played important roles in biological processes of apoptosis and cell motility. Additionally, some of the dysregulated genes participated in cellular components expression, forming such as cell membrane structure, extracellular matrix and collagen components. Conclusions Key genes including TGFB1, FN1, COL1A1, MMP9, VEGFA, TP53, IL6, and MMP2, along with TGF-β signal transduction, cell proliferation and apoptosis, tumor formation may play important roles in the development of keloid.
出处
《中国微创外科杂志》
CSCD
2012年第5期444-449,467,共7页
Chinese Journal of Minimally Invasive Surgery
基金
国家自然科学基金项目(30973126)
