Diet and Atherosclerosis in Apolipoprotein E-Deficient Mice

Imaizumi, Kazunori

doi:10.1271/bbb.110059

Cited by 30 publications

(20 citation statements)

References 148 publications

(126 reference statements)

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“…Accumulating evidence from animal studies has revealed that ApoE is a key protein in atherosclerosis via its role in inflammation, control of cholesterol, and blood pressure (24). A previous study demonstrated that Hp can interact with ApoE in a mechanism by which inflammation affects atherosclerotic progression (25).…”

Section: Discussionmentioning

confidence: 99%

Proteomic analysis of changes in protein expression in serum from animals exposed to paraquat

Kim

Jung

Gil

et al. 2012

International Journal of Molecular Medicine

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Abstract. Paraquat (PQ) poisoning remains a major public health concern in many countries. Extensive research has focused on finding early diagnostic biomarkers of acute PQ poisoning. In order to investigate the characterization of diagnostic biomarkers in PQ poisoning, we utilized proteomic analysis using serum from rats exposed to PQ, and we identified 8 differentially expressed proteins from over 500 protein spots. The expression of apolipoprotein E (ApoE), preprohaptoglobin (Pphg), a precursor of haptoglobin (Hp), and complement component 3 (C3) proteins was greatly induced by PQ exposure while the expression of fibrinogen γ-chain (FGG) and Ac-158 was dramatically reduced. To further investigate the possibility of ApoE, Pphg and FGG as useful diagnostic biomarkers of PQ poisoning, western blot and qRT-PCR analyses were conducted using cell lines as well as rat and human sera. The expression levels of ApoE, Hp and FGG were significantly altered in the presence of PQ in both rat and human serum suggesting that these proteins may be appropriate candidate molecular biomarkers for the early diagnosis of acute PQ intoxication.

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Section: Discussionmentioning

confidence: 99%

Proteomic analysis of changes in protein expression in serum from animals exposed to paraquat

Kim

Jung

Gil

et al. 2012

International Journal of Molecular Medicine

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“…Elimination of ApoE in this model causes severe hypercholesterolemia leading to spontaneous development of atherosclerosis [48,49].…”

Section: Role Of Apolipoprotein E and Ldls In Macrophage Polarizationmentioning

confidence: 91%

Microenviromental factors controlling macrophage polarization in atherosclerosis

Pello¹

2011

Endocrinol Metab Syndr

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Macrophages are critical for the initiation and perpetuation of intravascular inflammation through their ability to produce an array of cytokines and chemokines, to generate reactive oxygen species, and to process and present antigens to CD4 + T cells. Macrophages constitute a heterogeneous population of cells that are distinctly activated by various microenvironmental signals; however, the mechanisms contributing to the generation of distinct macrophage phenotypes in the context of atherosclerosis remain unclear. This review summarizes the well-characterized factors that govern macrophage polarization toward a specific phenotype and function. Understanding the microenviromental factors that control macrophage polarization and the precise roles of distinct macrophage subsets could provide the basis for novel treatment strategies aimed at limiting the progression of atherosclerosis.

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“…Apolipoprotein E is synthesized by several tissues, primarily the liver, brain, adrenal glands, adipose tissue, kidney and macrophages [28–30]. APOE associates with triglyceride-rich proteins such as VLDL and chylomicrons as well as a subset of high-density lipoproteins (HDL) [31, 32].…”

Section: Biological Functions Of Apolipoprotein Ementioning

confidence: 99%

Crossroads between peripheral atherosclerosis, western-type diet and skeletal muscle pathophysiology: emphasis on apolipoprotein E deficiency and peripheral arterial disease

Sfyri

Matsakas

2017

J Biomed Sci

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Atherosclerosis is a chronic inflammatory process that, in the presence of hyperlipidaemia, promotes the formation of atheromatous plaques in large vessels of the cardiovascular system. It also affects peripheral arteries with major implications for a number of other non-vascular tissues such as the skeletal muscle, the liver and the kidney. The aim of this review is to critically discuss and assimilate current knowledge on the impact of peripheral atherosclerosis and its implications on skeletal muscle homeostasis. Accumulating data suggests that manifestations of peripheral atherosclerosis in skeletal muscle originates in a combination of increased i)-oxidative stress, ii)-inflammation, iii)-mitochondrial deficits, iv)-altered myofibre morphology and fibrosis, v)-chronic ischemia followed by impaired oxygen supply, vi)-reduced capillary density, vii)- proteolysis and viii)-apoptosis. These structural, biochemical and pathophysiological alterations impact on skeletal muscle metabolic and physiologic homeostasis and its capacity to generate force, which further affects the individual’s quality of life. Particular emphasis is given on two major areas representing basic and applied science respectively: a)-the abundant evidence from a well-recognised atherogenic model; the Apolipoprotein E deficient mouse and the role of a western-type diet and b)-on skeletal myopathy and oxidative stress-induced myofibre damage from human studies on peripheral arterial disease. A significant source of reactive oxygen species production and oxidative stress in cardiovascular disease is the family of NADPH oxidases that contribute to several pathologies. Finally, strategies targeting NADPH oxidases in skeletal muscle in an attempt to attenuate cellular oxidative stress are highlighted, providing a better understanding of the crossroads between peripheral atherosclerosis and skeletal muscle pathophysiology.

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Diet and Atherosclerosis in Apolipoprotein E-Deficient Mice

Cited by 30 publications

References 148 publications

Proteomic analysis of changes in protein expression in serum from animals exposed to paraquat

Proteomic analysis of changes in protein expression in serum from animals exposed to paraquat

Microenviromental factors controlling macrophage polarization in atherosclerosis

Crossroads between peripheral atherosclerosis, western-type diet and skeletal muscle pathophysiology: emphasis on apolipoprotein E deficiency and peripheral arterial disease

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