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.