A time-course microarray data analysis reveals consistent dysregulated genes and upstream microRNAs in autoantibody-medi
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RESEARCH ARTICLE
Open Access
A time-course microarray data analysis reveals consistent dysregulated genes and upstream microRNAs in autoantibodymediated arthritis Xinwen Wang1, Jie Bai1, Zhen Jia2, Yangjun Zhu1, Jijun Liu1, Kun Zhang1, Dingjun Hao1 and Lisong Heng1*
Abstract Background: The purpose of this study is to identify key genes and microRNAs (miRNAs) involved in autoantibodymediated arthritis (AMA). Methods: A time-course microarray data (ID: GSE27492) of peripheral blood leukocytes, ankle tissue, and synovial fluid from K/BxN mouse serum-transferred mice were downloaded from Gene Expression Omnibus. Those samples were collected at days 0, 1, 3, 7, 12, and 18 after serum injection. Limma of R was employed to identify differentially expressed genes (DEGs) in samples collected at days 1–18 compared with those collected at day 0. Consistent DEGs were obtained by taking the interaction of DEGs from different time points, followed by functional enrichment analysis. MiRNAs were screened out and constructed into regulatory network with DEGs using Cytoscape. Results: In total, 17 consistent DEGs were obtained, including downregulated Ephx1 and upregulated AF251705, Adam8, Arg1, Basp1, Ccl2, Ccl7, Ccl9, Ccr2, Clec4a2, Clec4d, Cxcl1, Fabp5, Fcgr1, Gp49a, Il1rn, and Saa3. Those DEGs were associated with biological processes of immune response, inflammatory response, and defense response; chemokine signaling pathway; cytokine-cytokine receptor interaction; and NOD-like receptor signaling pathway. Additionally, 202 miRNAs were identified to have a regulatory effect on 9 of the 17 DEGs. Notably, miR-944, miR-374a, and miR374b were found to regulate the expression of Cxcl1, Ccl7, and Ccl2. Clec4d was targeted by 78 miRNAs. Conclusions: Our study reveals that 17 DEGs and 202 miRNAs may be associated with autoimmune disorder in the progression of AMA, which could guide future researches. Keywords: Arthritis, Differentially expressed genes, MicroRNA, Regulatory network
Background Rheumatoid arthritis (RA) is an autoimmune disease, which is characterized by inflammation of the joints and surrounding tissues and destruction of bone and cartilage [1]. Inflammatory response and immune response are found to play critical roles in the pathogenesis of RA [2–4]. Many cytokines have been implicated in the pathogenesis of arthritis, such as interleukin-1 * Correspondence: [email protected] 1 Department of Orthopedics, Honghui Hospital, Xi’an Jiaotong University, 555 East Youyi Road, Xi’an 710054, Shaanxi, People’s Republic of China Full list of author information is available at the end of the article
(IL-1) [5], IL-6 [6], IL-18 [7], and CC motif chemokine ligand 13 [8]. Matrix metalloproteinases (MMPs) play key roles in the destructive process and thus are also implicated in arthritis [9], especially MMP-1 and MMP-13. Those uncovered genes demonstrate an involvement of the gene factor in the progression of arthritis. Mouse models with autoantibody-mediated arthritis (AMA) are widely used in researches of arthritis [10].
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