RGD Reference Report - Deletion of bone marrow-derived receptor for advanced glycation end products inhibits atherosclerotic plaque progression. - Rat Genome Database

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Deletion of bone marrow-derived receptor for advanced glycation end products inhibits atherosclerotic plaque progression.

Authors: Morris-Rosenfeld, S  Blessing, E  Preusch, MR  Albrecht, C  Bierhaus, A  Andrassy, M  Nawroth, PP  Rosenfeld, ME  Katus, HA  Bea, F 
Citation: Morris-Rosenfeld S, etal., Eur J Clin Invest. 2011 Nov;41(11):1164-71. doi: 10.1111/j.1365-2362.2011.02514.x. Epub 2011 Mar 21.
RGD ID: 6784515
Pubmed: PMID:21418204   (View Abstract at PubMed)
DOI: DOI:10.1111/j.1365-2362.2011.02514.x   (Journal Full-text)

BACKGROUND: The multiligand receptor for advanced glycation end products (RAGE) of the immunoglobulin superfamily is expressed on multiple cell types implicated in the inflammatory response in atherosclerosis. We sought to determine the role of bone marrow-derived RAGE in different stages of atherosclerotic development in apolipoprotein E-deficient mice (apoE(-/-)). METHODS: Seven- and 23-week-old apoE(-/-) mice (n = 40) were lethally irradiated and given bone marrow from RAGE null (RAGE(-/-)/apoE(-/-)) or RAGE-bearing (RAGE(+/+)/apoE(-/-)) mice to apoE(-/-) mice to generate double knockout bone marrow chimera (RAGE(-/-)/apoE(-/-bmc) and RAGE(+/+)/apoE(-/-bmc)-, respectively). After 16 weeks on a standard chow diet, mice were sacrificed and atherosclerotic lesion formation was evaluated. RESULTS: Plaques in the aortic root of the young mice showed no significant difference in maximum plaque size (217,470 +/- 17,480 mum(2) for the RAGE(-/-) /apoE(-/-bmc) mice compared to 244,764 +/- 45,840 mum(2)), whereas lesions in the brachiocephalic arteries of the older RAGE(-/-)/apoE(-/-bmc) mice had significantly smaller lesions (94,049 +/- 13,0844 mum(2) vs. 145,570 +/- 11,488 mum(2), P < 0.05) as well as reduced average necrotic core area (48,600 +/- 9220 mum(2) compared to 89,502 +/- 10,032 mum(2), P < 0.05) when compared to RAGE(+/+)/apoE(-/-bmc) mice. Reduced plaque size and more stable plaque morphology was associated with significant reduced expression of VCAM-1, ICAM-1 and MCP-1. Accumulation of the RAGE ligand HMGB-1 was also significantly reduced within the lesions of RAGE(-/-)/apoE(-/-bmc) mice. CONCLUSIONS: This study demonstrates that bone marrow-derived RAGE is an important factor in the progression of atherosclerotic plaques.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
atherosclerosis  ISOAger (Mus musculus)6784515; 6784515 RGD 
atherosclerosis  IMP 6784515 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ager  (advanced glycosylation end product-specific receptor)

Genes (Mus musculus)
Ager  (advanced glycosylation end product-specific receptor)

Genes (Homo sapiens)
AGER  (advanced glycosylation end-product specific receptor)


Additional Information