期刊
MICROBIAL PATHOGENESIS
卷 69-70, 期 -, 页码 1-8出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.micpath.2014.03.001
关键词
Chlamydia pneumoniae; Foam cells; Peroxisome proliferator-activated receptors; Mitogen-activated protein kinase; Atherosclerosis
资金
- National Natural Science Foundation of China [30900599]
- Fundamental Research Funds for the Central Universities of China [2012QN228]
Chlamydia pneumoniae (C pneumoniae) is now widely accepted as an independent risk of atherosclerosis development. In this paper, our results showed that C. pneumoniae infection significantly increased the number of foam cells in LDL-treated THP-1 macrophages. C-Jun NH2 terminal kinase (JNK1/2) inhibitor SP600125 and extracellular signal-regulated kinase (ERK1/2) inhibitor PD98059 strongly inhibited C pneumoniae-induced accumulation of lipid droplet, whereas p38 inhibitor SB203580 had no obvious effect on lipid accumulation. Furthermore, we found that C pneumoniae not only stimulated the phosphorylation of Mitogen-activated protein kinase (MAPK) including JNK1/2, ERK1/2 and p38 but also down-regulated the expression of peroxisome proliferator-activated receptors (PPAR gamma and PPAR alpha) at mRNA and protein levels. However, the phosphorylation of JNK1/2, ERK1/2 and p38 MAPK by C pneumoniae was substantially reversed after PPAR gamma agonist (rosiglitazone) or PPAR alpha agonist (fenofibrate) treatment while PPAR gamma inhibitor (GW9662) and PPAR alpha antagonist (MK886) enhanced C pneumoniae-induced phosphorylation of JNK1/2, ERK1/2 and p38. In addition, we demonstrated that C pneumoniae-induced PPAR gamma and PPARa down-regulation were significantly suppressed by JNK1/2 inhibitor (SP600125) and ERK1/2 inhibitor (PD98059), but not p38 inhibitor (SB203580). These results first declare that MAPK-PPAR alpha/gamma reciprocal signal pathways are involved in C pneumoniae, which induces foam cell formation, thus facilitating atherogenesis. (C) 2014 Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据