Department of Orthopaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Hyogo, 650-0017, Japan.
Division of Orthopedic Science, Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Suma, Kobe, Hyogo, 654-0142, Japan.
Mol Biol Rep. 2024 Feb 24;51(1):356. doi: 10.1007/s11033-024-09311-0.
Synovial hyperplasia caused by rheumatoid arthritis (RA), an autoimmune inflammatory disease, leads to the destruction of the articular cartilage and bone. A member of the tumor necrosis factor superfamily, Lymphotoxin-related inducible ligand that competes for glycoprotein D binding to herpes virus entry mediator on T cells (LIGHT) has been shown to correlate with the pathogenesis of RA.
We used cDNA microarray analysis to compare the expression of genes in rheumatoid fibroblast-like synoviocytes with and without LIGHT stimulation.
Significant changes in gene expression (P-values < 0.05 and fold change ≥ 2.0) were associated mainly with biological function categories of glycoprotein, glycosylation site as N-linked, plasma membrane part, integral to plasma membrane, intrinsic to plasma membrane, signal, plasma membrane, signal peptide, alternative splicing, and topological domain as extracellular.
Our results indicate that LIGHT may regulate the expression in RA-FLS of genes which are important in the differentiation of several cell types and in cellular functions.
类风湿关节炎（RA）是一种自身免疫性炎症疾病，可导致滑膜增生，进而破坏关节软骨和骨骼。肿瘤坏死因子超家族的一个成员，与 RA 发病机制相关的淋巴毒素相关诱导配体，可竞争与 T 细胞上的疱疹病毒进入介质结合的糖蛋白 D（LIGHT）。
我们使用 cDNA 微阵列分析比较了有和没有 LIGHT 刺激的类风湿成纤维样滑膜细胞中基因的表达。
基因表达的显著变化（P 值 < 0.05，倍数变化≥2.0）主要与糖蛋白、N-连接糖基化位点、质膜部分、质膜整合、质膜固有、信号、质膜、信号肽、选择性剪接和拓扑结构作为细胞外等生物学功能类别相关。
我们的结果表明，LIGHT 可能调节 RA-FLS 中几个细胞类型分化和细胞功能相关基因的表达。
