SR-BI in Bone Marrow Derived Cells Protects Mice from Diet Induced Coronary Artery Atherosclerosis and Myocardial Infarction

Pei, Ying; Chen, Xing; Aboutouk, Dina; Fuller, Mark; Dadoo, Omid; Yu, Pei; White, Edward L.; Igdoura, Suleiman A.; Trigatti, Bernardo L.

doi:10.1371/journal.pone.0072492

Cited by 25 publications

(27 citation statements)

References 56 publications

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“…This appears to be attributable to deficient expression of this isoform in macrophages and increased macrophage lipoprotein uptake, likely mediated by pinocytosis 74 . This is in contrast to the attenuation of this phenotype upon transplantation of Srb1 expressing bone marrow into the hypomorphic apoE mice 75 , suggesting that SBR1 expression on bone marrow derived cells protects against coronary artery atherosclerosis. This suggests that SRB1 expressed in either macrophages or endothelial cells may contribute in a complex way to the coronary artery lesions.…”

Section: Coronary Artery Atherosclerosismentioning

confidence: 67%

Do the Apoe ^−/− and Ldlr ^−/– Mice Yield the Same Insight on Atherogenesis?

Getz

Reardon

2016

ATVB

151

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Murine models of atherosclerosis are useful for investigating the environmental and genetic influences on lesion formation and composition. Apoe−/− and Ldlr−/− are the two models most extensively used models. The models differ in important ways with respect to the precise mechanism by which their absence enhances atherosclerosis, including differences in plasma lipoproteins. The majority of the gene function studies have utilized only one model, with the results being generalized to atherogenic mechanisms. In only a relatively few cases have studies been conducted in both atherogenic murine models. This review will discuss important differences between the two atherogenic models and will point out studies that have been performed in the two models where results are comparable and those where different results were obtained.

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Section: Coronary Artery Atherosclerosismentioning

confidence: 67%

Do the Apoe ^−/− and Ldlr ^−/– Mice Yield the Same Insight on Atherogenesis?

Getz

Reardon

2016

ATVB

151

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“…SR‐BI/LDLR knockout mice fed a high‐cholesterol diet were more prone to develop atherosclerosis, MI and myocardial fibrosis than LDLR knockout mice fed the same diet (Fuller et al, ; Liao et al, ). SR‐BI knockout/Apo‐E hypomorphic mice showed the same characteristics, but when the animals were transplanted with bone marrow cells that express SR‐BI, the monocyte recruitment was attenuated, levels of IL‐6 were lower in plasma and the animals showed less atherosclerosis, MI, and cardiac fibrosis (Pei et al, ). Pagler et al () showed that SR‐BI is a mediator to the retroendocytosis of HDL and LDL, and the resecretion of HDL particle contributes to cholesterol efflux.…”

Section: Discussionmentioning

confidence: 99%

The Expression of Lipoprotein Receptors Is Increased in the Infarcted Area After Myocardial Infarction Induced in Rats With Cardiac Dysfunction

Lima

Guido

Tavares

et al. 2018

Lipids

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Left ventricular (LV) remodeling after myocardial infarction constitutes the structural basis for ventricular dysfunction and heart failure. The characterization underlying the expression of lipoprotein receptors in cardiac dysfunction is scarcely explored. The aim of this study was to analyze the status of lipoprotein receptors on the infarcted and noninfarcted areas of LV and to verify whether nanoparticles that mimic the lipid structure of low-density lipoprotein (LDL) and have the ability to bind to LDL receptors (LDE) are taken up more avidly by the noninfarcted LV. 13 male Wistar rats with left coronary artery ligation (myocardial infarction [MI]) and 12 animals with SHAM operation (SHAM) were used in this study. 6 weeks after the procedure, the quantification of low-density lipoprotein receptor (LDLR), LDL receptor-related protein 1 (LRP1), scavenger receptor-class B type I (SR-BI) lipoprotein receptors, and PCNA proliferation marker, and tissue uptake of radioactively labeled LDE were performed. Immunohistochemistry and Western blot analysis showed that LDLR, LRP1, SR-BI, and PCNA, expression in infarcted area of MI was remarkably higher than SHAM and noninfarcted subendocardial (SEN) and interstitial (INT) areas. In addition, in SEN noninfarcted area of MI, the presence of LDLR was about threefold higher than in SHAM SEN and INT noninfarcted areas. The LDE uptake of noninfarcted LV of MI group was about 30% greater than that of SHAM group. In conclusion, these findings regarding the status of lipoprotein receptors after MI induction could help to establish mechanisms on myocardial repairing. In conclusion, infarcted rats with LV dysfunction showed increased expression of lipoprotein receptors mainly in the infarcted area.

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“…We have previously demonstrated that monocyte recruitment into atherosclerotic plaques is attenuated by restoration of SR-BI expression in the bone marrow of SR-BI knockout/apoE hypomorphic mice, and that SR-BI-deficient monocytes bind VCAM-1 and ICAM-1 more readily than SR-BI-expressing monocytes. 29 Monocytes can be divided into subsets based on their level of Ly6C expression. Ly6C hi monocytes are considered to be more inflammatory, adhere more efficiently to activated endothelium, migrate more efficiently into established atherosclerotic plaques, and selectively accumulate in atherosclerotic plaques compared with Ly6C lo monocytes.…”

Section: Fuller Et Al Coronary Atherosclerosis In Sr-bi/ldlr Dko Micementioning

confidence: 99%

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

Fuller

Dadoo

Serkis

et al. 2014

ATVB

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The HDL receptor, scavenger receptor class B type I (SR-BI), is expressed on the surface of multiple cell types and has been shown to mediate both HDL-dependent atheroprotective © 2014 American Heart Association, Inc.Arterioscler Thromb Vasc Biol is available at http://atvb.ahajournals.org DOI: 10.1161/ATVBAHA.114.304200Objective-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 Fuller et al Coronary Atherosclerosis in SR-BI/LDLR dKO Mice 2395signaling 8,9 and selective lipid transfer between HDL and cells, which is critical for functional reverse cholesterol transport, the major avenue for cholesterol removal from peripheral tissues.8,10 Deficiency of SR-BI not only accelerates atherosclerosis in the aortic sinus of apoE knockout mice 11 but also renders these mice susceptible to spontaneous occlusive CA atherosclerosis, myocardial infarction, and ultimately early death. 12 A related model, the SR-BI knockout/apoE hypomorphic mouse, develops a similar phenotype when fed high fat, high cholesterol (HFC) diets. 13,14 We have previously shown that SR-BI deficiency increases atherosclerosis in the aortas of LDLR knockout mice fed a high-fat (HF) Western-type diet; however, reduced survival was not observed in these mice, and CA atherosclerosis was not assessed. 15In the current study, we tested the effects of feeding SR-BI/ LDLR double knockout (dKO) mic...

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SR-BI in Bone Marrow Derived Cells Protects Mice from Diet Induced Coronary Artery Atherosclerosis and Myocardial Infarction

Cited by 25 publications

References 56 publications

Do the Apoe ^−/− and Ldlr ^−/– Mice Yield the Same Insight on Atherogenesis?

Do the Apoe ^−/− and Ldlr ^−/– Mice Yield the Same Insight on Atherogenesis?

The Expression of Lipoprotein Receptors Is Increased in the Infarcted Area After Myocardial Infarction Induced in Rats With Cardiac Dysfunction

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

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SR-BI in Bone Marrow Derived Cells Protects Mice from Diet Induced Coronary Artery Atherosclerosis and Myocardial Infarction

Cited by 25 publications

References 56 publications

Do the Apoe −/− and Ldlr −/– Mice Yield the Same Insight on Atherogenesis?

Do the Apoe −/− and Ldlr −/– Mice Yield the Same Insight on Atherogenesis?

The Expression of Lipoprotein Receptors Is Increased in the Infarcted Area After Myocardial Infarction Induced in Rats With Cardiac Dysfunction

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

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Do the Apoe ^−/− and Ldlr ^−/– Mice Yield the Same Insight on Atherogenesis?

Do the Apoe ^−/− and Ldlr ^−/– Mice Yield the Same Insight on Atherogenesis?