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A neutralizing antibody against receptor for advanced glycation end products (RAGE) reduces atherosclerosis in uremic mice.

Abstract：

: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<0.001). In plasma, the RAGE-ab reduced concentrations of oxidized phospholipid neo-epitopes in plasma as detected by the specific monoclonal antibody EO6 (P<0.05) and titers of IgG antibodies against oxidized low-density lipoprotein (P<0.001). In the aorta of treated mice, the RAGE-ab did not affect the mRNA expression of eight selected genes associated with inflammation. The results suggest that blockade of RAGE reduces the proatherogenic effects of uremia, possibly through a systemic decrease in oxidative stress.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Bro S,Flyvbjerg A,Binder CJ,Bang CA,Denner L,Olgaard K,Nielsen LB

doi

10.1016/j.atherosclerosis.2008.01.015

subject

Has Abstract

pub_date

2008-12-01 00:00:00

pages

274-80

issue

2

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(08)00078-6

journal_volume

201

pub_type

杂志文章

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