TWEAK can induce pro-inflammatory cytokines and matrix metalloproteinase-9 in macrophages
TWEAK can induce pro-inflammatory cytokines and matrix metalloproteinase-9 in macrophages
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DOI：
10.1253/circj.68.396
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发表时间：
2004-04-01
影响因子：
3.3
通讯作者：
Lee, WH
中科院分区：
文献类型：
--
作者：
Kim, SH;Kang, YJ;Lee, WH
在动脉粥样硬化斑块中巨噬细胞/泡沫细胞丰富的区域检测到TWEAK （TNFSF12）和TWEAK r /Fn14的表达。通过分析TWEAK在人巨噬细胞样细胞系THP-1中诱导的细胞事件，研究了TWEAK在单核细胞中与动脉粥样硬化相关的作用。TWEAK诱导了多种动脉粥样硬化分子介质，如IL-6、MCP-1、IL-8和MMP-9，并通过干扰素- γ增强了诱导作用。tweak诱导的MMP-9活化是通过NF-kappaB活化介导的。这些结果表明，TWEAK通过诱导促炎细胞因子和细胞外基质降解酶参与动脉粥样硬化，从而降低斑块稳定性。
The expression of TWEAK (TNFSF12) and TweakR/Fn14 was detected in regions rich in macrophage/foarn cells in atherosclerotic plaques. The role of TWEAK in monocytes in relation to atherogenesis was investigated by analyzing the cellular events induced by TWEAK in a human macrophage-like cell line, THP-1. TWEAK induced various molecular mediators of atherogenesis, such as IL-6, MCP-1, IL-8 and MMP-9, and the induction was augmented by interferon-gamma. TWEAK-induced activation of MMP-9 was mediated by activation of NF-kappaB. These results suggest that TWEAK is involved in atherosclerosis by inducing pro-inflammatory cytokines and extracellular matrix degrading enzymes, which reduce plaque stability.