Increased ICAM-1 and PECAM-1 transcription levels in the heart of Apo-E deficient mice in comparison to wild type (C57BL6).

被引:0
作者
Zibara, K
Chettab, K
McGregor, B
Poston, R
McGregor, J
机构
[1] Thrombosis Res Inst, Post Genom Atherothrombosis Lab, London SW3 6LR, England
[2] Fac Med RTH Laennec, U331, INSERM, F-69008 Lyon, France
[3] Guys Hosp, UMDS, Dept Expt Pathol, London, England
关键词
atherosclerosis; adhesion molecules; apolipoprotein E; knockout mice; heart; northern;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Adhesion molecules and chemoattractants are thought to play a critical role in the homing of leukocytes to sites of vascular lesions. Apo-E deficiency in mice creates an atherosclerotic model that mimics vascular lesions in man. Little is known on the effect of Apo-E deficiency on expression of adhesion molecules in the hearts of these animals. In this study, male C57BL6 and Apo-E deficient mice were fed a chow diet over periods of time (0 to 20 weeks). The transcription levels of major adhesion molecules (ICAM-1. PECAM-1), present in the heart, were followed by northern blots. Immunohistochemistry was used to localize these adhesion molecules in the heart. Results show a significant increase in gene transcription levels of ICAM-1 and PECAM-1 in Apo-E animals, but not wild type, at 16 and 20 weeks of chow dirt. Such increase in levels of transcription was not observed in younger Apo-E and C57BL6 animals (0, 6 weeks of diet). ICAM-1 and PECAM-1 were strongly expressed in the endocardium and heart microvessels. In contrast, VCAM-1 was poorly stained, with only an occasional expression on the endocardium and arterioles. Enhanced gene expression levels of heart ICAM-1 and PECAM-1 observed in Apo-E deficient mice. but not in control animals, appears to induce the initial stages of an inflammatory reaction. Such observations. not previously reported, may induce heart vascular remodeling.
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页码:908 / 914
页数:7
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