Galectin-3 Is an Amplifier of Inflammation in Atherosclerotic Plaque Progression Through Macrophage Activation And Monocyte Chemoattraction

OBJECTIVE—Galectin-3 (Gal-3) is a 26-kDa lectin known to regulate many aspects of inflammatory cell behavior. We assessed the hypothesis that increased levels of Gal-3 contribute to atherosclerotic plaque progression by enhancing monocyte chemoattraction through macrophage activation. METHODS AND RE...

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Veröffentlicht in:	Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2008-03, Vol.28 (3), p.433-440
Hauptverfasser:	Papaspyridonos, Marianna, McNeill, Eileen, de Bono, Joe P, Smith, Alberto, Burnand, Kevin G, Channon, Keith M, Greaves, David R
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Atherosclerosis (general aspects, experimental research) Biological and medical sciences Biomarkers - metabolism Blood and lymphatic vessels Blotting, Western Cardiology. Vascular system Carotid Arteries - metabolism Carotid Arteries - pathology Carotid Stenosis - metabolism Cells, Cultured Chemotaxis - physiology Coronary heart disease Disease Models, Animal Disease Progression Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Galectin 3 - metabolism Heart Humans Immunohistochemistry Inflammation - metabolism Macrophage Activation Macrophages - cytology Macrophages - metabolism Medical sciences Mice Mice, Inbred C57BL Monocytes - cytology Monocytes - metabolism Random Allocation RNA - analysis Sensitivity and Specificity Up-Regulation
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Zusammenfassung:	OBJECTIVE—Galectin-3 (Gal-3) is a 26-kDa lectin known to regulate many aspects of inflammatory cell behavior. We assessed the hypothesis that increased levels of Gal-3 contribute to atherosclerotic plaque progression by enhancing monocyte chemoattraction through macrophage activation. METHODS AND RESULTS—Gal-3 was found to be upregulated in unstable plaque regions of carotid endarterectomy (CEA) specimens compared with stable regions from the same patient (3.2-fold, P
ISSN:	1079-5642 1524-4636
DOI:	10.1161/ATVBAHA.107.159160