关键词: Bioinformatics Fibroblast Interleukin-7 Osteoarthritis Rheumatoid arthritis Synovium

来  源:   DOI:10.1016/j.heliyon.2024.e28330   PDF(Pubmed)

Abstract:
UNASSIGNED: OA was generally considered as a non-inflammatory disease dominated by articular cartilage degeneration. However, the role of synovitis in OA pathogenesis has received increasing attention. Recent studies support that OA patients have a pro-inflammatory/catabolic synovial environment similar to RA patients, promoting the occurrence and development of OA. Therefore, we investigated the co-immune-related genes and pathways of OA and RA to explore whether part of the pathogenesis of RA synovitis can be used to explain OA synovitis.
UNASSIGNED: Data of GSE29746 and GSE12021 were downloaded from the Gene Expression Omnibus (GEO) database. Compared with control group, differentially expressed genes (DEGs) of OA and RA groups were screened separately by R software, Venny website was used to screen co-DEGs. Metascape was used to screen the common enriched terms and pathways between OA and RA. STRING website and Cytoscape software were used to map protein-protein interaction (PPI) networks and screen co-hub genes. GSE29746 was selected as the test dataset, and GSE12021 as the validation dataset for validate the co-hub genes. The results were validated by western blotting (WB) and real-time quantitative polymerase chain reaction (qPCR) of clinical synovial samples.
UNASSIGNED: We identified 573 OA-related DEGs, 148 RA-related DEGs, and 52 co-DEGs, revealing 14 common enriched terms, most of which were related to immune inflammation. IL7R was the only upregulated co-hub gene between OA and RA in the PPI network, consistent with the validation dataset. IL7R was highly expressed in clinical osteoarthritic synovial samples (P < 0.001).
UNASSIGNED: Our findings suggested that IL7R is a critical co-DEG in OA and RA and confirmed the involvement of immune inflammation in disease pathogenesis. Furthermore, it confirms the role of IL7R in synovial inflammation in RA and OA synovitis and provides evidence for further investigation of OA immune inflammation.
摘要:
OA通常被认为是以关节软骨退变为主的非炎性疾病。然而,滑膜炎在OA发病机制中的作用日益受到重视。最近的研究支持OA患者具有与RA患者相似的促炎/分解代谢滑膜环境,促进OA的发生和发展。因此,我们研究了OA和RA的共同免疫相关基因和途径,以探讨RA滑膜炎的部分发病机制是否可用于解释OA滑膜炎.
从基因表达综合(GEO)数据库下载GSE29746和GSE12021的数据。与对照组相比,用R软件分别筛选OA和RA组的差异表达基因(DEGs),Venny网站用于筛选联合DEG。Metascape用于筛选OA和RA之间常见的富集术语和途径。STRING网站和Cytoscape软件用于绘制蛋白质-蛋白质相互作用(PPI)网络并筛选co-hub基因。选择GSE29746作为测试数据集,和GSE12021作为验证共集线器基因的验证数据集。通过临床滑膜样品的蛋白质印迹(WB)和实时定量聚合酶链反应(qPCR)验证结果。
我们确定了573个与OA相关的DEG,148个RA相关DEG,和52个共同DEG,揭示了14个常见的丰富术语,其中大部分与免疫炎症有关。IL7R是PPI网络中OA和RA之间唯一上调的共中心基因,与验证数据集一致。IL7R在临床骨关节炎滑膜样品中高度表达(P<0.001)。
我们的研究结果表明,IL7R是OA和RA中的关键协同DEG,并证实了免疫炎症参与疾病的发病机理。此外,它证实了IL7R在RA和OA滑膜炎滑膜炎中的作用,并为进一步研究OA免疫炎症提供了证据。
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