Determination of molecular pathways and gene ontology of genes associated with Raynaud’s phenomenon

Gözde Öztan
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Abstract

Abstract Objectives Raynaud’s phenomenon (RF) is a disease that causes discoloration of the fingers. The purpose of this study is to identify the molecular pathways in which genes related to RP illness are involved, as well as uncover the biological processes and molecular functions connected with those genes via the use of gene ontology (GO) analysis. Methods Genes associated with RP in the MalaCards Human Diseases database were detected. Twenty genes obtained from the MalaCards Human Diseases database were included in the study for gene ontology analysis via the STRING database. Accordingly, possible interactions between 20 genes were determined through STRING and network enrichment was performed. Results A significant enrichment by gene ontology enrichment analysis was detected in a subset of genes involved in biological processes including cellular response to luteinizing hormone stimulus, negative regulation of fibrinolysis, negative regulation of smooth muscle cell apoptotic process, plasminogen activation, cellular response to follicle-stimulating hormone stimulus. The assay for molecular function determined enrichment of a subset of genes in chemoattractant activity, growth factor activity, heparin binding, sulfur compound binding, growth factor receptor binding. Through the use of KEGG pathways, we were able to identify many molecular processes that contribute to RP, including the AGE-RAGE signaling pathway in diabetic complications, complement and coagulation cascades, fluid shear stress, atherosclerosis. Conclusions Some individuals may have a genetic predisposition to the onset of Raynaud’s phenomenon. Our data showed that it is associated with genes involved in vascular damage and fibrosis, especially in RP. Therefore, we can include RP disease in the group of vascular diseases.
确定雷诺现象相关基因的分子通路和基因本体论
摘要 目的 雷诺现象(Raynaud's phenomenon,RF)是一种导致手指变色的疾病。本研究旨在通过基因本体(GO)分析,确定雷诺氏病相关基因参与的分子通路,并揭示与这些基因相关的生物学过程和分子功能。方法 在 MalaCards 人类疾病数据库中检测与 RP 相关的基因。研究通过 STRING 数据库对从 MalaCards 人类疾病数据库中获得的 20 个基因进行了基因本体分析。因此,通过 STRING 确定了 20 个基因之间可能存在的相互作用,并进行了网络富集。结果 通过基因本体富集分析,发现涉及细胞对黄体生成素刺激的反应、纤维蛋白溶解的负调控、平滑肌细胞凋亡过程的负调控、纤溶酶原激活、细胞对卵泡刺激素刺激的反应等生物过程的基因子集有明显的富集。分子功能检测确定了化合吸引剂活性、生长因子活性、肝素结合、硫化合物结合、生长因子受体结合等方面的基因子集富集。通过使用 KEGG 通路,我们能够确定许多导致 RP 的分子过程,包括糖尿病并发症中的 AGE-RAGE 信号通路、补体和凝血级联、流体剪切应力、动脉粥样硬化。结论 某些人可能具有雷诺现象发病的遗传易感性。我们的数据显示,雷诺现象与涉及血管损伤和纤维化的基因有关,特别是在雷诺氏病中。因此,我们可以将雷诺氏病纳入血管疾病的范畴。
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