期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 32, 期 5, 页码 1265-1274出版社
KARGER
DOI: 10.1159/000354525
关键词
Macrophages; Interleukin 17A; Inflammatory cytokines
资金
- National Basic Research Program of China [973 Program] [2013CB531103, 2012CB517805]
- National Natural Science Foundation of China [81170303, 81222002]
- Program for New Century Excellent Talents in University of China [NCET-09-0380]
Background: Interleukin (IL)-17A, a newly identified cytokine, may participate in the transition of a stable plaque into an unstable plaque. Macrophages play a critical role in the destabilization of atherosclerotic plaque. Methods: RAW 264.7 cells were stimulated with IL-17A. The mRNA expression of inflammatory cytokines was determined by RT-PCR. The cytokines production in the supernatants was measured by ELISA. Small interfering RNA (siRNA) was used to confirm that IL-17A-induced pro-inflammatory cytokines production via IL-17RA signaling. The western blot assay was used to detect the phosphorylation of MAPKinases including p38 and ERK1/2. The DNA binding activity of nuclear factor NF-kappa B and AP-1 were detected by EMSA. Results: IL-17A induced the production of pro-inflammatory cytokines in macrophages in a time-and dose-dependent manner, such as tumor necrosis factor (TNF)-alpha, IL-1 beta, and IL-6. Meanwhile, IL-17A resulted in the phosphorylation of p38 and ERK1/2 and increased DNA-binding activity of NF-kappa B and AP-1. Pharmacological inhibitors of p38 and ERK1/2 partly attenuated IL-17A-induced TNF-alpha, IL-1 beta, and IL-6 production. Either NF-kappa B inhibitor or AP-1 inhibitor also partly decreased the IL-17A-induced cytokine production. Conclusions: IL-17A induces pro-inflammatory cytokines production in macrophages via MAPKinases, NF-kappa B and AP-1 pathway. Copyright (C) 2013 S. Karger AG, Basel
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