Atherosclerosis

2010

DOI: 10.1016/j.atherosclerosis.2010.04.027

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Chronic infusion of salusin-α and -β exerts opposite effects on atherosclerotic lesion development in apolipoprotein E-deficient mice

Masaharu Nagashima

¹

,

Takuya Watanabe

²

,

³

et al.

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Cited by 55 publications

(79 citation statements)

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“…Shown are effects on aortic root atherosclerosis of 4 wk infusion starting at 13 wk. Macrophage CD36 expression was upregulated (1270). 1230% LXR has multiple effects both on both macrophage scavenger receptor expression and lipoprotein uptake and efflux.…”

Section: Nsmentioning

confidence: 97%

Molecular Biology of Atherosclerosis

¹

2013

Physiological Reviews

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At least 468 individual genes have been manipulated by molecular methods to study their effects on the initiation, promotion, and progression of atherosclerosis. Most clinicians and many investigators, even in related disciplines, find many of these genes and the related pathways entirely foreign. Medical schools generally do not attempt to incorporate the relevant molecular biology into their curriculum. A number of key signaling pathways are highly relevant to atherogenesis and are presented to provide a context for the gene manipulations summarized herein. The pathways include the following: the insulin receptor (and other receptor tyrosine kinases); Ras and MAPK activation; TNF-␣ and related family members leading to activation of NF-B; effects of reactive oxygen species (ROS) on signaling; endothelial adaptations to flow including G protein-coupled receptor (GPCR) and integrin-related signaling; activation of endothelial and other cells by modified lipoproteins; purinergic signaling; control of leukocyte adhesion to endothelium, migration, and further activation; foam cell formation; and macrophage and vascular smooth muscle cell signaling related to proliferation, efferocytosis, and apoptosis. This review is intended primarily as an introduction to these key signaling pathways. They have become the focus of modern atherosclerosis research and will undoubtedly provide a rich resource for future innovation toward intervention and prevention of the number one cause of death in the modern world.

“…Shown are effects on aortic root atherosclerosis of 4 wk infusion starting at 13 wk. Macrophage CD36 expression was upregulated (1270). 1230% LXR has multiple effects both on both macrophage scavenger receptor expression and lipoprotein uptake and efflux.…”

Section: Nsmentioning

confidence: 97%

Molecular Biology of Atherosclerosis

¹

2013

Physiological Reviews

View full text Add to dashboard Cite

At least 468 individual genes have been manipulated by molecular methods to study their effects on the initiation, promotion, and progression of atherosclerosis. Most clinicians and many investigators, even in related disciplines, find many of these genes and the related pathways entirely foreign. Medical schools generally do not attempt to incorporate the relevant molecular biology into their curriculum. A number of key signaling pathways are highly relevant to atherogenesis and are presented to provide a context for the gene manipulations summarized herein. The pathways include the following: the insulin receptor (and other receptor tyrosine kinases); Ras and MAPK activation; TNF-␣ and related family members leading to activation of NF-B; effects of reactive oxygen species (ROS) on signaling; endothelial adaptations to flow including G protein-coupled receptor (GPCR) and integrin-related signaling; activation of endothelial and other cells by modified lipoproteins; purinergic signaling; control of leukocyte adhesion to endothelium, migration, and further activation; foam cell formation; and macrophage and vascular smooth muscle cell signaling related to proliferation, efferocytosis, and apoptosis. This review is intended primarily as an introduction to these key signaling pathways. They have become the focus of modern atherosclerosis research and will undoubtedly provide a rich resource for future innovation toward intervention and prevention of the number one cause of death in the modern world.

“…caused a signifi cant reduction of cholesterol accumulation in macrophages by downregulating SR-A, LOX-1, and ACAT1 expression and upregulating ABCA1 expression, of which ACAT1 and ABCA1 are considered to be candidate targets for the treatment of atherosclerotic lesions due to their roles in macrophage cholesterol metabolism ( 18,(52)(53)(54)(55). ACAT1 inhibition or downregulation was shown to be atheroprotective in animal models ( 18,(56)(57)(58). ABCA1 acts as the primary gatekeeper for eliminating excess tissue cholesterol and represents the first and rate-controlling step in reverse cholesterol transport ( 59,60 ).…”

Section: Discussionmentioning

confidence: 99%

Specific Kv1.3 blockade modulates key cholesterol-metabolism-associated molecules in human macrophages exposed to ox-LDL

¹

,

²

,

³

et al. 2013

Journal of Lipid Research

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Atherosclerosis contributes chiefl y to ischemic diseases, including coronary heart disease, cerebral infarction, and intermittent claudication. Lipid plaque is the main pathological presentation and is characterized by abundant foam cells, which are derived mostly from macrophages. In the transformation, cholesterol ester accumulation accelerates foam cell formation.Macrophages possess an entrance-to-exit machinery for the modulation of cholesterol metabolism. Scavenger receptor class A (SR-A), CD36, and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) are largely responsible for cholesterol infl ux ( 1-8 ), and ABCA1, ABCG1 and scavenger receptor class B type I (SR-B I) facilitate cholesterol effl ux ( 9-15 ). Free cholesterol inside macrophages is esterifi ed by ACAT1, thereby promoting cholesterol ester accumulation ( 16-18 ). All the molecules form an integrated modulating Abstract Cholesterol-metabolism-associated molecules, including scavenger receptor class A (SR-A), lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), CD36, ACAT1, ABCA1, ABCG1, and scavenger receptor class B type I, can modulate cholesterol metabolism in the transformation from macrophages to foam cells. Voltage-gated potassium channel Kv1.3 has increasingly been demonstrated to play an important role in the modulation of macrophage function. Here, we investigate the role of Kv1.3 in modulating cholesterol-metabolism-associated molecules in human acute monocytic leukemia cell-derived macrophages (THP-1 macrophages) and human monocyte-derived macrophages exposed to oxidized LDL (ox-LDL). Human Kv1.3 and Kv1.5 channels (hKv1.3 and hKv1.5) are expressed in macrophages and form a heteromultimeric channel. The hKv1.3-E314 antibody that we had generated as a specifi c hKv1.3 blocker inhibited outward delayed rectifi er potassium currents, whereas the hKv1.5-E313 antibody that we had generated as a specifi c hKv1.5 blocker failed. Accordingly, the hKv1.3-E314 antibody reduced percentage of cholesterol ester and enhanced apoA-I-mediated cholesterol effl ux in THP-1 macrophages and human monocyte-derived macrophages exposed to ox-LDL. The hKv1.3-E314 antibody downregulated SR-A, LOX-1, and ACAT1 expression and upregulated ABCA1 expression in THP-1 macrophages and human monocyte-derived macrophages. Our results reveal that specifi c Kv1.3 blockade represents a novel strategy modulating cholesterol metabolism in macrophages, which benefi ts the treatment of atherosclerotic lesions. Press, October 24, 2012 DOI 10.1194 Specifi c Kv1.3 blockade modulates key cholesterol-metabolism-associated molecules in human macrophages exposed to ox-LDL Published, JLR Papers in

“…Three groups of 17-week-old ApoE −/− mice were infused with recombinant human CT-1 (100 μg/kg per day; BioVendor, Modrice, Czech Republic), antimouse CT-1-neutralizing antibody (10 μg/kg per day; R&D Systems), or saline (vehicle) for 4 weeks by osmotic mini-pumps (Alzet Model 1002; Durect, Cupertino, CA). 3,[22][23][24][25] In our preliminary examination, 4-week infusion of recombinant human CT-1 at different doses brought a result that its plasma concentration increased by 7-fold (0.96±0.77 to 6.87±1.71 ng/mL) at 100 μg/kg per day in ApoE −/− mice.…”

Section: Animal Experimentsmentioning

confidence: 99%

“…Plasma concentrations of glucose and total cholesterol were measured by enzymatic methods using an autoanalyzer (Hitachi, Tokyo). [23][24][25] Plasma CT-1 concentration was measured by ELISA (ELISA kit for human CT-1; Antigenix America, Huntington Station, NY).…”

Section: Animal Measurementsmentioning

confidence: 99%

Stimulatory Effects of Cardiotrophin 1 on Atherosclerosis

¹

,

Sato²,

et al. 2013

Self Cite

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A therosclerosis is a pathological injury-to-response process that is initiated by early inflammatory responses of vascular endothelial cells (ECs).1 Endothelial inflammation is characterized by increased production of proatherogenic molecules and inflammatory cytokines in ECs, and monocyte adhesion and infiltration into the neointima lesion, followed by oxidized low-density lipoprotein-induced transformation of macrophages into foam cells.2 Accumulation of cholesterol ester in macrophages is a hallmark of foam cell formation. 2This accumulation depends on the balance between the uptake of oxidized low-density lipoprotein via CD36 and the efflux of free cholesterol controlled by ATP-binding cassette transporter A1 (ABCA1), ATP-binding cassette transporter G1, or scavenger receptor class B type I (SR-BI).3 To protect the cells from the toxicity that would result from excessive free cholesterol accumulation, the free cholesterol is esterified to cholesterol ester by acyl-CoA:cholesterol acyltransferase-1 (ACAT1).3 Cholesterol ester stored in lipid droplets can be removed from cells only after hydrolysis to free cholesterol by neutral cholesterol ester hydrolase. 4 Apart from accumulation of macrophage-derived foam cells, the migration and proliferation of vascular smooth muscle cells (VSMCs) followed by extracellular matrix (ECM) production play crucial roles in the development of atherosclerotic lesions. 1Cardiotrophin 1 (CT-1), a 201-aa member of the interleukin-6 cytokine family, was originally cloned from embryoid bodies as a 21.5-kDa protein capable of inducing hypertrophy in neonatal cardiomyocytes. 5 Human and mouse CT-1 share 80% amino acid sequence identity and exhibit cross-species activity.6 Subsequent studies confirmed that plasma concentrations of CT-1 are elevated in various cardiorenal diseases, such as hypertension, ischemic heart disease, heart failure, and chronic renal disease.7-10 CT-1 exerts cardiovascular remodeling induced by hypertensive and ischemic heart diseases and congestive heart failure, through its receptor complex glycoprotein 130 (gp130) and leukemia inhibitory factor receptor (LIFR).11-14 Recently, CT-1 has been shown to be expressed in the intima in the early stages of atherosclerotic lesions in human carotid artery.15 CT-1 stimulates the synthesis of inflammatory cytokines and proatherogenic molecules, such as interleukin-6, Abstract-Cardiotrophin 1 (CT-1), an interleukin-6 family cytokine, was recently shown to be expressed in the intima of early atherosclerotic lesions in the human carotid artery. CT-1 stimulates proatherogenic molecule expression in human vascular endothelial cells and monocyte migration. However, it has not been reported whether CT-1 accelerates atherosclerosis. This study was performed to examine the stimulatory effects of CT-1 on human macrophage foam cell formation and vascular smooth muscle cell migration and proliferation in vitro, and on the development of atherosclerotic lesions in apolipoprotein E-deficient (ApoE −/− ) mice in vivo. CT-1 was express...

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