School of Oral Hygiene, College of Oral Medicine, Taipei Medical University, Taipei City, Taiwan.
Chronic Disease and Health Promotion Research Center, Chang Gung University of Science and Technology, Taoyuan, Chiayi County, Taiwan.
J Cell Physiol. 2021 Mar;236(3):2205-2213. doi: 10.1002/jcp.30009. Epub 2020 Aug 17.
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.
骨关节炎（OA）是一种以滑膜炎症为特征的进行性退行性关节疾病。白细胞介素 6（IL-6）是 OA 进展中的关键促炎细胞因子。细颗粒物 2.5（PM2.5）暴露会增加患不同疾病的风险，包括 OA。到目前为止，还没有研究描述过 PM2.5 与人类 OA 滑膜成纤维细胞（OASFs）中 IL-6 表达之间的任何关联。在这里，我们的数据表明，PM2.5 浓度和时间依赖性地促进了人类 OASFs 中 IL-6 的合成。我们还发现，活性氧（ROS）的产生增强了 PM2.5 对 IL-6 产生的影响。ASK1、ERK、p38 和 JNK 抑制剂降低了 PM2.5 诱导的 IL-6 表达增加。用 PM2.5 处理 OASFs 促进了这些信号通路的磷酸化。我们还发现，PM2.5 增强了 c-Jun 的磷酸化及其向核内的易位。因此，PM2.5 通过 ROS、ASK1、ERK、p38、JNK 和 AP-1 信号通路增加人类 OASFs 中 IL-6 的产生。我们的证据将 PM2.5 与 OA 进展联系起来。
