1. A neutralizing antibody against receptor for advanced glycation end products (RAGE) reduces atherosclerosis in uremic mice
- Author
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Klaus Olgaard, Christoph J. Binder, Christian Axel Bang, Allan Flyvbjerg, Susanne Bro, Larry Denner, and Lars Nielsen
- Subjects
Apolipoprotein E ,Male ,medicine.medical_specialty ,Apolipoprotein B ,endocrine system diseases ,Receptor for Advanced Glycation End Products ,Vascular Cell Adhesion Molecule-1 ,Inflammation ,Antibodies ,RAGE (receptor) ,Epitopes ,Mice ,Glycation ,Internal medicine ,medicine ,Animals ,Receptors, Immunologic ,Neutralizing antibody ,Aorta ,Uremia ,biology ,business.industry ,Reverse Transcriptase Polymerase Chain Reaction ,nutritional and metabolic diseases ,medicine.disease ,Atherosclerosis ,Mice, Inbred C57BL ,Oxidative Stress ,Endocrinology ,biology.protein ,cardiovascular system ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,business ,Lipoprotein ,Signal Transduction - Abstract
Udgivelsesdato: 2008-Dec Chronic renal failure markedly accelerates atherogenesis in apolipoprotein E-deficient (apoE(-/-)) mice. To study the putative role of receptor for advanced glycation end products (RAGE) in development of uremic atherosclerosis, apoE(-/-) mice received intraperitoneal injections thrice weekly of a neutralizing murine RAGE-antibody (RAGE-ab) (n=21) or an isotype-matched control antibody (placebo-ab) (n=23). Treatment was started 4 weeks after surgical 5/6 nephrectomy in 16 weeks old mice and continued for 12 weeks. The RAGE-ab did not affect blood pressure, plasma cholesterol or measures of uremia. However, the aortic plaque area fraction was reduced by 59% in RAGE-ab compared with placebo-ab-treated mice (0.016 +/- 0.002 versus 0.039 +/- 0.005, P
- Published
- 2007
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