The Effects of Diet on Occlusive Coronary Artery Atherosclerosis and Myocardial Infarction in Scavenger Receptor Class B, Type 1/Low-Density Lipoprotein Receptor Double Knockout Mice

被引:59
作者
Fuller, Mark [1 ,4 ,5 ]
Dadoo, Omid [1 ,4 ,5 ]
Serkis, Viktoria [1 ,4 ,5 ]
Abutouk, Dina [1 ]
MacDonald, Melissa [1 ,4 ,5 ]
Dhingani, Neel [1 ,4 ,5 ]
Macri, Joseph [2 ]
Igdoura, Suleiman A. [2 ,3 ]
Trigatti, Bernardo L. [1 ,4 ,5 ]
机构
[1] McMaster Univ, Dept Biochem & Biomed Sci, Hamilton, ON L8N 3Z5, Canada
[2] McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON L8N 3Z5, Canada
[3] McMaster Univ, Dept Biol, Hamilton, ON L8N 3Z5, Canada
[4] Hamilton Hlth Sci, Thrombosis & Atherosclerosis Res Inst, Hamilton, ON, Canada
[5] McMaster Univ, Hamilton, ON L8N 3Z5, Canada
基金
加拿大健康研究院; 加拿大自然科学与工程研究理事会;
关键词
atherosclerosis; HDL; receptors; lipoprotein; thrombosis; NITRIC-OXIDE SYNTHASE; E-DEFICIENT MICE; MARROW-DERIVED CELLS; SR-BI; APOLIPOPROTEIN-E; PREMATURE DEATH; CARDIAC DYSFUNCTION; LESION DEVELOPMENT; ENDOTHELIAL-CELLS; TARGETED MUTATION;
D O I
10.1161/ATVBAHA.114.304200
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective Deficiency of the high-density lipoprotein receptor, scavenger receptor class B, type I (SR-BI), in apolipoprotein E knockout or hypomorphic mice, respectively, results in spontaneous or diet-inducible occlusive coronary artery (CA) atherosclerosis, myocardial infarction, and early death. Here, we examine effects of SR-BI deficiency on cardiovascular phenotypes in low-density lipoprotein receptor (LDLR) knockout mice fed different atherogenic diets. Approach and Results SR-BI/LDLR double knockout and control LDLR knockout mice were fed atherogenic diets containing different amounts of fat, cholesterol, and sodium cholate. Double knockout mice fed atherogenic diets high in cholesterol exhibited significantly reduced survival compared with LDLR knockout mice fed the same diets. In addition to increased diet-accelerated aortic sinus atherosclerosis, we observed significant diet-induced CA atherosclerosis in double knockout mice and diet-dependent accumulation of platelets in CA atherosclerotic plaques. This was accompanied by substantial myocardial fibrosis in double knockout mice fed high cholesterol diets. Atherogenic diet fed double knockout mice also exhibited higher circulating cytokine levels, monocytosis with increased proportions of Ly6C(hi) and Ly6C(int) monocytes, and higher adhesion molecule expression in CA endothelial cells compared with control LDLR knockout mice. Conclusions Diet-accelerated atherosclerosis and occlusive, platelet-rich CA disease in SR-BI/LDLR double knockout mice is affected by amounts of cholesterol and cholate in atherogenic diets and is accompanied by increased expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 in CAs and increased Ly6C(hi) and Ly6C(int) monocytes in circulation. The increased vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 in CA endothelial cells in SR-BI-deficient mice likely explains their increased susceptibility to atherosclerosis in CAs.
引用
收藏
页码:2394 / 2403
页数:10
相关论文
共 42 条
[1]   A role for the scavenger receptor, class B type I in high density lipoprotein dependent activation of cellular signaling pathways [J].
Al-Jarallah, Aishah ;
Trigatti, Bernardo L. .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS, 2010, 1801 (12) :1239-1248
[2]   Probucol prevents early coronary heart disease and death in the high-density lipoprotein receptor SR-BI/apolipoprotein E double knockout mouse [J].
Braun, A ;
Zhang, SW ;
Miettinen, HE ;
Ebrahim, S ;
Holm, TM ;
Vasile, E ;
Post, MJ ;
Yoerger, DM ;
Picard, MH ;
Krieger, JL ;
Andrews, NC ;
Simons, M ;
Krieger, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (12) :7283-7288
[3]   Loss of SR-BI expression leads to the early onset of occlusive atherosclerotic coronary artery disease, spontaneous myocardial infarctions, severe cardiac dysfunction, and premature death in apolipoprotein E-deficient mice [J].
Braun, A ;
Trigatti, BL ;
Post, MJ ;
Sato, K ;
Simons, M ;
Edelberg, JM ;
Rosenberg, RD ;
Schrenzel, M ;
Krieger, M .
CIRCULATION RESEARCH, 2002, 90 (03) :270-276
[4]   SR-BI protects against endotoxemia in mice through its roles in glucocorticoid production and hepatic clearance [J].
Cai, Lei ;
Ji, Ailing ;
de Beer, Frederick C. ;
Tannock, Lisa R. ;
van der Westhuyzen, Deneys R. .
JOURNAL OF CLINICAL INVESTIGATION, 2008, 118 (01) :364-375
[5]   Macrophage SR-BI regulates LPS-induced pro-inflammatory signaling in mice and isolated macrophages [J].
Cai, Lei ;
Wang, Zhen ;
Meyer, Jason M. ;
Ji, Ailing ;
van der Westhuyzen, Deneys R. .
JOURNAL OF LIPID RESEARCH, 2012, 53 (08) :1472-1481
[6]   Scavenger receptor class B type I-mediated protection against atherosclerosis in LDL receptor-negative mice involves its expression in bone marrow-derived cells [J].
Covey, SD ;
Krieger, M ;
Wang, W ;
Penman, M ;
Trigatti, BL .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2003, 23 (09) :1589-1594
[7]   Deficiency of Scavenger Receptor BI Leads to Impaired Lymphocyte Homeostasis and Autoimmune Disorders in Mice [J].
Feng, Hong ;
Guo, Ling ;
Wang, Dan ;
Gao, Haiqing ;
Hou, Guihua ;
Zheng, Zhong ;
Ai, Junting ;
Foreman, Oded ;
Daugherty, Alan ;
Li, Xiang-An .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2011, 31 (11) :2543-U454
[8]   Vascular adhesion molecules in atherosclerosis [J].
Galkina, Elena ;
Ley, Klaus .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2007, 27 (11) :2292-2301
[9]   Scavenger Receptor BI Protects against Septic Death through Its Role in Modulating Inflammatory Response [J].
Guo, Ling ;
Song, Zhiqing ;
Li, Mengting ;
Wu, Qingan ;
Wang, Dan ;
Feng, Hong ;
Bernard, Philip ;
Daugherty, Alan ;
Huang, Bin ;
Li, Xiang-An .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (30) :19826-19834
[10]   The NF-κB signal transduction pathway in aortic endothelial cells is primed for activation in regions predisposed to atherosclerotic lesion formation [J].
Hajra, L ;
Evans, AI ;
Chen, M ;
Hyduk, SJ ;
Collins, T ;
Cybulsky, MI .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (16) :9052-9057