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PM2.5 facilitates IL‐6 production in human osteoarthritis synovial fibroblasts via ASK1 activation
Author(s) -
Liu JuFang,
Chi MiaoChing,
Lin ChihYang,
Lee ChiangWen,
Chang TsungMing,
Han ChienKuo,
Huang YuanLi,
Fong YiChin,
Chen HsienTe,
Tang ChihHsin
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.30009
Subject(s) - p38 mitogen activated protein kinases , proinflammatory cytokine , inflammation , phosphorylation , mapk/erk pathway , microbiology and biotechnology , cancer research , ask1 , reactive oxygen species , signal transduction , chemistry , interleukin , cytokine , medicine , immunology , biology , protein kinase a , mitogen activated protein kinase kinase
Osteoarthritis (OA) is a progressive degenerative joint disorder characterized by synovial inflammation. Interleukin‐6 (IL‐6) is a key proinflammatory cytokine in OA progression. Particulate matter 2.5 (PM2.5) exposure increases the risk of different diseases, including OA. Up until now, no studies have described any association between PM2.5 and IL‐6 expression in human OA synovial fibroblasts (OASFs). Here, our data show that PM2.5 concentration‐ and time‐dependently promoted IL‐6 synthesis in human OASFs. We also found that reactive oxygen species (ROS) generation potentiated the effects of PM2.5 on IL‐6 production. ASK1, ERK, p38, and JNK inhibitors reduced PM2.5‐induced increases of IL‐6 expression. Treatment of OASFs with PM2.5 promoted phosphorylation of these signaling cascades. We also found that PM2.5 enhanced c‐Jun phosphorylation and its translocation into the nucleus. Thus, PM2.5 increases IL‐6 production in human OASFs via the ROS, ASK1, ERK, p38, JNK, and AP‐1 signaling pathways. Our evidence links PM2.5 with OA progression.