CD5L induces inflammation and survival in RA-FLS through ERK1/2 MAPK pathway

作者全名："Yang, Huiqing; Luo, Yan; Lai, Xiaofei"

作者地址："[Yang, Huiqing; Luo, Yan; Lai, Xiaofei] Chongqing Med Univ, Affiliated Hosp 1, Dept Lab Med, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China"

通信作者："Lai, XF (通讯作者)，Chongqing Med Univ, Affiliated Hosp 1, Dept Lab Med, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China."

来源：AUTOIMMUNITY

ESI学科分类：IMMUNOLOGY

WOS号：WOS:001176334300001

JCR分区：Q3

影响因子：3.3

年份：2024

卷号：57

期号：1

开始页：　

结束页：　

文献类型：Article

关键词：CD5L; rheumatoid arthritis; inflammatory factors; signalling pathway; proliferation

摘要："ObjectiveTo explore the effect of CD5-like molecule (CD5L) on rheumatoid arthritis (RA) fibroblast-like synoviocytes (RA-FLS) and the relative molecular mechanism of CD5L in it.MethodsRecombinant protein CD5L was used to stimulate the cultured RA-FLS cells. The inflammation-related cytokines were determined by real time-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The signal molecules and apoptosis-related molecules were detected by western blot assay (WB), and cell counting kit-8 (CCK-8) was used to detect the proliferation.ResultsCD5L can increase the production of IL-6, IL-8, and TNF-alpha and this effect can be inhibited by signal pathway inhibitor. At the same time, CD5L activated ERK1/2 MAPK signal, inhibitor treatment can weaken the intensity of phosphorylation. In addition, CD5L can enhance the proliferation ability of RA-FLS.ConclusionCD5L induces the production of inflammatory cytokines in RA-FLS through the ERK1/2 MAPK pathway and increases cell survival."

基金机构：National Natural Science Foundation of China; Medical Experimental Center of the First Affiliated Hospital of Chongqing Medical University

基金资助正文：We thank the Clinical Laboratory of the Department of Medical Laboratory and the Medical Experimental Center of the First Affiliated Hospital of Chongqing Medical University for their equipment and technical support.