Study on up-regulation of the expression of cholesterol acyltransferase 1 induced by chlamydia pneumoniae via c-Jun N-terminal kinase signal transduction pathway
10.3760/cma.j.issn.0254-9026.2009.10.015
- VernacularTitle:肺炎衣原体通过c-jun氨基末端激酶信号通路上调胆固醇酰基转移酶1的表达
- Author:
Wei LIU
;
Ping HE
;
Bei CHENG
;
Chunli MEI
;
Yanfu WANG
;
Jingjing WAN
- Publication Type:Journal Article
- Keywords:
Chlamydophila pneumoniae;
JNK mitogen-activated protein kinases;
Acyl Coenzyem A;
Foam cells
- From:
Chinese Journal of Geriatrics
2009;28(10):851-855
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of c-Jun N-terminal kinase (JNK) signal transduction pathway on the up-regulation of the expression of acyl-coenzyme A: cholesterol acyltransferasel (ACAT1) induced by Chlamydia pneumoniae (C. pn), and to discuss the mechanism of macrophages-derived foam cell formation induced by C. pn. Methods C. pn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA) for 48 h, and were randomly allocated into four groups to be incubated continually: control group, C. pn infection group, C. pn and SP600125 (a special JNK inhibitor)group and SP600125 group. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellular cholesterol ester were detected by enzyme fluorescence analysis. The expressions of ACAT1 mRNA and protein were determined by reverse transcriptase polymerase chain reaction(RT-PCR) and Western blot, respectively. Results Compared with the control group, the expressions of ACAT1 mRNA and protein were up-regulated in C. pn infection group [(4.16±0.26) vs. (2.17±0.18), (1.20±0.10)vs. (0.61±0.03), both P<0.05], and C. pn-induced foam cell formation was observed. The expressions of ACAT1 mRNA and protein and the foam cell formation were inhibited by SP600125 in a concentration-dependent manner (r = - 0.92, P<0.05; r= - 0. 96, P<0.05, respectively). Conclusions The up-regulation of ACAT1 expression is induced by C. pn via JNK signal transduction pathway, which is involved in the mechanism of C. pn-induced macrophage-derived foam cell formation.
