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

Citation
K. Zibara et al., Increased ICAM-1 and PECAM-1 transcription levels in the heart of Apo-E deficient mice in comparison to wild type (C57BL6)., THROMB HAEM, 85(5), 2001, pp. 908-914
Citations number
40
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
THROMBOSIS AND HAEMOSTASIS
ISSN journal
03406245 → ACNP
Volume
85
Issue
5
Year of publication
2001
Pages
908 - 914
Database
ISI
SICI code
0340-6245(200105)85:5<908:IIAPTL>2.0.ZU;2-S
Abstract
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 m an. Little is known on the effect of Apo-E deficiency on expression of adhe sion molecules in the hearts of these animals. In this study, male C57BL6 a nd 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. Immunohistochem istry was used to localize these adhesion molecules in the heart. Results s how 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. Su ch increase in levels of transcription was not observed in younger Apo-E an d C57BL6 animals (0, 6 weeks of diet). ICAM-1 and PECAM-1 were strongly exp ressed in the endocardium and heart microvessels. In contrast, VCAM-1 was p oorly stained, with only an occasional expression on the endocardium and ar terioles. Enhanced gene expression levels of heart ICAM-1 and PECAM-1 obser ved in Apo-E deficient mice. but not in control animals, appears to induce the initial stages of an inflammatory reaction. Such observations. not prev iously reported, may induce heart vascular remodeling.