TXNDC5 在类风湿关节炎成纤维样滑膜细胞中上调 CXCL10 和 TRAIL。
CXCL10 and TRAIL Are Upregulated by TXNDC5 in Rheumatoid Arthritis Fibroblast-like Synoviocytes.
机构信息
From the Medical Research Center of Shandong Provincial Qianfoshan Hospital, Shandong University; Department of Bone and Joint Surgery of Shandong Provincial Hospital, Shandong University; Department of Bone Surgery of Shandong Provincial Qianfoshan Hospital, Shandong University, Shandong, China.
B. Xu, PhD, Medical Research Center of Shandong Provincial Qianfoshan Hospital, Shandong University; J. Li, MSc, Medical Research Center of Shandong Provincial Qianfoshan Hospital, Shandong University; C. Wu, MD, PhD, Department of Bone and Joint Surgery of Shandong Provincial Hospital, Shandong University; C. Liu, PhD, Medical Research Center of Shandong Provincial Qianfoshan Hospital, Shandong University; X. Yan, MD, PhD, Department of Bone Surgery of Shandong Provincial Qianfoshan Hospital, Shandong University; X. Chang, MD, PhD, Medical Research Center of Shandong Provincial Qianfoshan Hospital, Shandong University. Bing Xu and Jian Li contributed equally to this work.
出版信息
J Rheumatol. 2018 Mar;45(3):335-340. doi: 10.3899/jrheum.170170. Epub 2017 Dec 15.
OBJECTIVE
Thioredoxin domain containing 5 (TXNDC5) is highly expressed in synovial membranes of rheumatoid arthritis (RA). Our study aimed to investigate the pathogenic role of TXNDC5 in RA.
METHODS
PCR arrays, CCK-8 assays, flow cytometry, and transwell migration assays were used to analyze cultured rheumatoid arthritis synovial fibroblasts (RASF).
RESULTS
Increased CXCL10 and tumor necrosis factor-related apoptosis-inducing ligand levels were detected in RASF transfected with anti-TXNDC5 small interfering RNA (siRNA), and decreased expression was detected in RASF transfected with TXNDC5-expressing plasmids. Significantly attenuated RASF proliferation and migration, and increased RASF apoptosis, were observed in the siRNA-transfected RASF.
CONCLUSION
Downregulation of TXNDC5 could contribute to RASF antiangiogenic and proapoptotic features through the suppression of CXCL10 and TRAIL (tumor necrosis factor-related apoptosis-inducing ligand).
目的
硫氧还蛋白结构域蛋白 5（TXNDC5）在类风湿关节炎（RA）的滑膜组织中高表达。本研究旨在探讨 TXNDC5 在 RA 中的致病作用。
方法
采用 PCR 阵列、CCK-8 检测、流式细胞术和 Transwell 迁移实验分析培养的类风湿关节炎滑膜成纤维细胞（RASF）。
结果
用抗 TXNDC5 小干扰 RNA（siRNA）转染的 RASF 中检测到 CXCL10 和肿瘤坏死因子相关凋亡诱导配体（TRAIL）水平升高，而用 TXNDC5 表达质粒转染的 RASF 中表达水平降低。在 siRNA 转染的 RASF 中，RASF 的增殖和迁移明显减弱，而凋亡增加。
结论
下调 TXNDC5 通过抑制 CXCL10 和 TRAIL（肿瘤坏死因子相关凋亡诱导配体），可能有助于 RASF 抗血管生成和促凋亡的特性。
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