Abstract
Background Keloid is a benign dermal tumor characterized by abnormal proliferation and invasion of fibroblasts. The establishment of biomarkers is essential for the diagnosis and treatment of keloids. Methods We systematically identified coexpression modules using the weighted gene coexpression network analysis method (WGCNA). Differential expressed genes (DEGs) in GSE145725 and genes in significant modules were integrated to identify overlapping key genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were then performed, as well as protein-protein interaction (PPI) network construction for hub gene screening. Results Using the R package of WGCNA, 22 coexpression modules consisting of different genes were identified from the top 5,000 genes with maximum mean absolute deviation in 19 human fibroblast samples. Blue-green and yellow modules were identified as the most important modules, where genes overlapping with DEGs were identified as key genes. We identified the most critical functions and pathways as extracellular structure organization, vascular smooth muscle contraction, and the cGMP-PKG signaling pathway. Hub genes from key genes as BMP4, MSX1, HAND2, TBX2, SIX1, IRX1, EDN1, DLX5, MEF2C, and DLX2 were identified. Conclusion The blue-green and yellow modules may play an important role in the pathogenesis of keloid. 10 hub genes were identified as potential biomarkers and therapeutic targets for keloid.
Highlights
Keloids are mainly associated with excessive proliferation of fibroblasts and massive deposition of the extracellular matrix following skin injury [1]. e clinical presentation of keloids is primarily a growth of scar tissue above the skin, usually accompanied by pruritus and pain [2]
Fibroblasts are the most abundant cells in the dermis and maintain dermal structure by producing an extracellular matrix (ECM) [7]. e ECM is in a constant state of synthesis, degradation, and remodeling, both under normal conditions and in the presence of disease or injury [8]
After a 2-3 d period of haemostasis and inflammation, the dermis undergoes a proliferative phase in which fibroblasts move from a homeostatic state to an activated state, where their ability to proliferate and migrate is significantly enhanced and they differentiate into a unique phenotype, myofibroblasts, which have stronger contractile properties and synthesized the ECM more rapidly, thereby accelerating wound closure [9]
Summary
Keloids are mainly associated with excessive proliferation of fibroblasts and massive deposition of the extracellular matrix following skin injury [1]. e clinical presentation of keloids is primarily a growth of scar tissue above the skin, usually accompanied by pruritus and pain [2]. Keloids are mainly associated with excessive proliferation of fibroblasts and massive deposition of the extracellular matrix following skin injury [1]. E treatment of keloid is not ideal because of unclear pathogenesis and regulatory mechanisms underlying keloids [5] For these reasons, the identification of hub genes involved in keloid is urgent and highly demanded for improving the clinical outcome. Fibroblasts are the most abundant cells in the dermis and maintain dermal structure by producing an extracellular matrix (ECM) [7]. The persistence of active fibroblasts (including myofibroblasts) at the site of Journal of Healthcare Engineering injury may lead to excessive deposition of the ECM and the formation of abnormal scarring. We systematically identified coexpression modules using the weighted gene coexpression network analysis method (WGCNA). Conclusion. e blue-green and yellow modules may play an important role in the pathogenesis of keloid. 10 hub genes were identified as potential biomarkers and therapeutic targets for keloid
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