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Title: Effect of Chlamydia pneumoniae infection and hyperlipidaemia on the expression of PPARγ, P50 and c-Fos in aortic endothelial cells in C57BL/6J mice
Author(s): HUANG, Bingsheng , DONG, Yugang , MAI, Weiyi , LI, Yongqiang
Journal: Acta Cardiologica
Volume: 60 Issue: 1 Date: February 2005
Objective — To investigate the effect of C. pneumoniae infection and/or hyperlipidaemia on the expression of peroxisome proliferator-activated receptor gamma (PPARγ), nuclear factor-kappa B (NF-kB) and activated protein-1 (AP-1) in aortic endothelial cells in C57BL/6J mice.
Methods and Results — Forty-eight, 8-week-old female C57BL/6J mice were divided into four groups: A, B, C and D (each twelve mice). Group A (as blank control) and B were fed a regular diet. Group C and D were fed an atherogenic diet (consisting of 15% fat, 2.5% cholesterol and 0.5% sodium cholate). Group B and D were infected with C. pneumoniae. Fourteen weeks later, the expression of PPARy, P50 (subunit of NF-kB) and c-Fos (subunit of AP-1) was determined by indirect immunofluorescence in the aortic endothelial cells. Slides of aortic sinus were prepared by cryosection, and stained with Sudan IV for examination of atherosclerotic plaque. The score of atherosclerotic plaque was determined by microscopy. The score of atherosclerotic plaque in group B was not increased, while it was significantly higher in groups C and D (P < 0.01), still the score in group D was higher than in group C (P < 0.01). The expression of PPARγ, NF-kB and AP-1 in endothelial cells in aortic sinus was upregulated in group B, C and D, in comparison with group A (P < 0.05). There was no significant difference among groups B, C and D.
Conclusion — The expression of PPARγ, NF-kB and AP-1 was upregulated in the endothelial cells in mice infected with C. pneumoniae and/or fed with an atherogenic diet. An atherogenic diet or this diet combined with C. pneumoniae infection accelerated the process of atherosclerosis. The diet infected with C. pneumoniae alone would not accelerate this process. PPARγ might play an anti-atherosclerotic role in this process.