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The role of bone marrow and non-bone marrow derived receptor for advanced glycation end products (RAGE) in a mouse model of diabetes-associated atherosclerosis.
MedLine Citation:
PMID:  24724734     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The receptor for advanced glycation end products (RAGE) is expressed on multiple cell types implicated in the progression of atherosclerosis and plays a role in diabetes-associated atherosclerosis (DAA). We aimed to determine the relative role of either bone marrow or non-bone marrow derived RAGE in the pathogenesis of streptozotocin (STZ)- DAA. Seven week old male ApoE null (ApoE-/-:RAGE+/+) and ApoE:RAGE null (ApoE-/-:RAGE-/-) mice were rendered diabetic with STZ. At eight weeks of age, ApoE-/- and ApoE-/-:RAGE-/- control and diabetic mice received bone marrow from either RAGE null or RAGE-bearing mice, generating various chimeras. After 10 and 20 weeks of diabetes, mice were sacrificed and gene expression and atherosclerotic lesion formation were evaluated, respectively. Deletion of RAGE in either the bone marrow cells or non-bone marrow cells both resulted in a significant attenuation in DAA which was associated with reduced VCAM-1 expression and translated to reduced adhesion in vitro. This study highlights the importance of both bone marrow and non-bone marrow derived RAGE in attenuating the development of DAA.
Authors:
Christine Koulis; Peter Kanellakis; Raelene J Pickering; Despina Tsorotes; Andrew J Murphy; Stephen P Gray; Merlin C Thomas; Karin A M Jandeleit-Dahm; Mark E Cooper; Terri J Allen
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-4-11
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  -     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2014 Apr 
Date Detail:
Created Date:  2014-4-14     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
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