Summary
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 diet. 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.
Keywords
Atherosclerosis - adhesion molecules - apolipoprotein E - knockout mice - heart -
northern
