The effects of IL-32 on the inflammatory activation of cultured rat primary astrocytes

被引:29
作者
Cho, Kyu Suk [2 ]
Park, Seung Hwa [2 ]
Joo, So Hyun [2 ]
Kim, Soo-Hyun [3 ]
Shin, Chan Young [1 ,2 ]
机构
[1] Konkuk Univ, Sch Med, Dept Pharmacol, IBST, Seoul 143701, South Korea
[2] Konkuk Univ, Sch Med, Dept Neurosci, Seoul 143701, South Korea
[3] Konkuk Univ, Dept Biomed Sci & Technol, Seoul 143701, South Korea
关键词
IL-32; iNOS; MMP-9; tPA; Inflammatory responses; Astrocyte; TISSUE-PLASMINOGEN ACTIVATOR; NITRIC-OXIDE SYNTHASE; CYTOKINE; INTERLEUKIN-32; MATRIX-METALLOPROTEINASE-9; EXPRESSION; IL-1-BETA; RESPONSES; DISEASE; KINASE;
D O I
10.1016/j.bbrc.2010.09.099
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
A new family of cytokine IL-32 has been implicated in pro-inflammatory immune responses several human diseases such as rheumatoid arthritis, inflammatory bowel diseases and vasculitis. In this study, we investigated the role of IL-32 in the inflammatory activation of cultured rat primary astrocytes. Treatment of IL-32 increased ROS production and augmented lipopolysaccharide-induced increased production of nitric oxide as well as the expression of iNOS. IL-32 also induced the expression of MMP-9 but not MMP-2 in rat primary astrocytes. The increased expression of these inflammatory mediators was accompanied by the increased mRNA expression encoding iNOS, MMP-9 and TNF-alpha. ERK1/2 and p38, two essential regulators of pro-inflammatory signaling in rat primary astrocytes were activated by IL-32 as evidenced by increased phosphorylation. The results from the present study suggest that IL-32 may play a role in the regulation of neuroinflammatory responses in several neurological disease conditions such as ischemia and Alzheimer's disease. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:48 / 53
页数:6
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