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

IF 4.3 3区材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC

ACS Applied Electronic Materials Pub Date : 2024-12-01 Epub Date: 2024-02-29 DOI:10.1080/08916934.2023.2201412

Huiqing Yang, Yan Luo, Xiaofei Lai

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引用次数: 0

Abstract

Objective: To 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.

Methods: Recombinant 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.

Results: CD5L can increase the production of IL-6, IL-8, and TNF-α 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.

Conclusion: CD5L induces the production of inflammatory cytokines in RA-FLS through the ERK1/2 MAPK pathway and increases cell survival.

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CD5L 通过 ERK1/2 MAPK 通路诱导 RA-FLS 的炎症和存活。

目的探讨CD5样分子（CD5L）对类风湿性关节炎（RA）成纤维细胞样滑膜细胞（RA-FLS）的影响及其相关分子机制：方法：使用重组蛋白 CD5L 刺激培养的 RA-FLS 细胞。方法：采用重组蛋白 CD5L 刺激培养的 RA-FLS 细胞，通过实时聚合酶链反应（RT-PCR）和酶联免疫吸附试验（ELISA）测定炎症相关细胞因子。信号分子和细胞凋亡相关分子采用免疫印迹法（WB）检测，细胞计数试剂盒-8（CCK-8）用于检测细胞增殖：结果：CD5L能增加IL-6、IL-8和TNF-α的产生，信号通路抑制剂能抑制这种效应。同时，CD5L激活ERK1/2 MAPK信号，抑制剂处理可减弱磷酸化强度。此外，CD5L还能增强RA-FLS的增殖能力：结论：CD5L可通过ERK1/2 MAPK途径诱导RA-FLS产生炎性细胞因子，并提高细胞存活率。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

ACS Applied Electronic Materials Multiple-

CiteScore

7.20

自引率

4.30%

发文量

567