Insulin-degrading enzyme deficiency in bone marrow cells increases atherosclerosis in LDL receptor-deficient mice

被引：12
作者：
Caravaggio, Justin W. [1 ,2 ]
Hasu, Mirela [1 ]
MacLaren, Robin [1 ]
Thabet, Mohamed [1 ]
Raizman, Joshua E. [1 ]
Veinot, John P. [1 ,3 ]
Marcel, Yves L. [1 ,3 ]
Milne, Ross W. [1 ,3 ]
Whitman, Stewart C. [1 ,2 ,3 ]
机构：
[1] Univ Ottawa, Inst Heart, Ottawa, ON K1Y 4W7, Canada
[2] Univ Ottawa, Dept Cellular & Mol Med, Ottawa, ON K1Y 4W7, Canada
[3] Univ Ottawa, Dept Pathol & Lab Med, Ottawa, ON K1Y 4W7, Canada
来源：
CARDIOVASCULAR PATHOLOGY | 2013年 / 22卷 / 06期
关键词：
Atherosclerosis; Insulin-degrading enzyme; LDL receptor-deficient mice; Bone marrow transplantation; Amyloid; Receptor for advanced glycation end products (RAGE); BLOOD-BRAIN-BARRIER; AMYLOID PRECURSOR PROTEIN; ALZHEIMERS-DISEASE; SCAVENGER RECEPTOR; UP-REGULATION; BETA-PEPTIDE; IN-VIVO; DEGRADATION; PRODUCTS; CLEARANCE;
D O I：
10.1016/j.carpath.2013.03.006
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Background: Insulin-degrading enzyme (IDE), a protease implicated in several chronic diseases, associates with the cytoplasmic domain of the macrophage Type A scavenger receptor (SR-A). Our goal was to investigate the effect of IDE deficiency (Ide(-/-)) on diet-induced atherosclerosis in low density lipoprotein-deficient (Ldlr(-/-)) mice and on SR-A function. Methods: Irradiated Ldlr(-/-) or Ide(-/-)Ldlr(-/-) mice were reconstituted with wild-type or Ide(-/-) bone marrow and, 6 weeks later, were placed on a high-fat diet for 8 weeks. Results: After 8 weeks on a high-fat diet, male Ldlr(-/-) recipients of Ide(-/-) bone marrow had more atherosclerosis, higher serum cholesterol and increased lesion-associated beta-amyloid, an IDE substrate, and receptor for advanced glycation end products (RAGE), a proinflammatory receptor for beta-amyloid, compared to male Ldlr(-/-) recipients of wild-type bone marrow. IDE deficiency in male Ldlr(-/-) recipient mice did not affect atherosclerosis or cholesterol levels and moderated the effects of IDE deficiency of bone marrow-derived cells. No differences were seen between Ldlr(-/-) and Ide(-/-)Ldlr(-/-) female mice reconstituted with Ide(-/-) or wild-type bone marrow. IDE deficiency in macrophages did not alter SR-A levels, cell surface SR-A, or foam cell formation. Conclusion: IDE deficiency in bone marrow-derived cells results in larger atherosclerotic lesions, increased lesion-associated A beta and RAGE, and higher serum cholesterol in male, Ldlr(-/-) mice. (C) 2013 Elsevier Inc. All rights reserved.
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收藏
页码：458 / 464
页数：7
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