Mechanism and Role of High Density Lipoprotein-induced Activation of AMP-activated Protein Kinase in Endothelial Cells

Kimura, Takao; Tomura, Hideaki; Sato, Kōichi; Ito, Masaaki; Matsuoka, Isao; Im, Doon Soon; Kuwabara, Atsushi; Mogi, Chihiro; Itoh, Hiroshi; Kurose, Hitoshi; Murakami, Masami; Okajima, Fumikazu

doi:10.1074/jbc.m109.043869

Cited by 70 publications

(54 citation statements)

References 54 publications

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“…There is also evidence that lipid-free apoA-I and recombinant HDL inhibit endothelial cell adhesion molecule expression by upregulating the expression of 3 ␤ -hydroxysteriod-⌬ 24 reductase (DHCR24) and heme oxygenase-1 (HO-1), with the increased expression by HO-1 being mediated by DHCR24 upregulation and resulting activation of PI3 kinase and Akt ( 61 ). Other studies have indicated that HDL activation of AMP-activated protein kinase (AMPK) is required in HDL modulation of adhesion molecule expression and that the signaling events proximal to AMPK involve calcium/calmodulin-dependent protein kinase kinase (CaMKK) and liver kinase B1 (LKB1) ( 62 ). Recognizing the key role of NF-B in the modulation of cellular responses to infl ammation, it has also been shown that apoA-I decreases NF-B activation induced by palmitate in cultured endothelial cells ( 63 ).…”

Section: Endothelial Cellsmentioning

confidence: 99%

Regulation of signal transduction by HDL

Mineo

Shaul

2013

Journal of Lipid Research

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which HDL serves to shuttle cholesterol from peripheral tissues or cells to the liver. This review highlights recent advances in our knowledge of HDL-initiated processes mediated by changes in intracellular signaling in numerous cell types of relevance to both cardiovascular and metabolic conditions, which represent actions of the lipoprotein beyond its classical role in global cholesterol homeostasis. The evidence that HDL infl uences cardiovascular and metabolic health and disease will fi rst be briefl y summarized. Responses to HDL or to apoA-I, its major apolipoprotein, in cellular targets directly involved in vascular biology will then be reviewed, followed by a summary of the mechanisms that HDL infl uences in cell types participating in energy and glucose homeostasis. The processes underlying apoA-I-or HDL-induced changes in intracellular signaling will then be discussed, and fi nally presently unanswered questions in this realm of HDL biology will be considered. Although HDL cargo molecules can contribute to cellular responses to the lipoprotein ( 1, 2 ), herein emphasis will be placed primarily on signaling events directly induced by apoA-I or HDL, which are likely occurring in response to cholesterol effl ux. To help leverage our present understanding of apoA-I-or HDL-initiated signaling in future studies, the signaling events and the proteins or mediators whose abundance or activity is altered by apoA-I or HDL in various cell types are summarized in Tables Abbreviations: AMPK, AMP-activated protein kinase; CaMKK, calcium/calmodulin-dependent protein kinase kinase; COX-2, cyclooxygenase type 2; DHCR24, 3 ␤ -hydroxysteriod-⌬ 24 reductase; eNOS, endothelial nitric-oxide synthase; EPC, endothelial progenitor cell; GKS3, glycogen synthase kinase 3; HO-1, heme oxygenase-1; ICAM-1, intercellular adhesion molecule-1; JAK2, Janus kinase 2; LKB1, liver kinase B1; MCP-1, monocyte chemoattractant protein-1; PKA, protein kinase A; PKC, protein kinase C; RCT, reverse cholesterol transport; ROS, reactive oxygen species; S1P, sphingosine-1-phosphate; SAA3, serum amyloid A3; SR-BI, scavenger receptor class B, type I; VCAM-1, vascular cell adhesion molecule-1; VSM, vascular smooth muscle.

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Section: Endothelial Cellsmentioning

confidence: 99%

Regulation of signal transduction by HDL

Mineo

Shaul

2013

Journal of Lipid Research

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“…Previous studies have focused on the individual involvement of either the SR-BI or S1PR receptor proteins in HDL-mediated biological effects or signaling pathways, but studies investigating the potential for both receptors to jointly mediate HDL-induced biological functions are limited (20,21). We have previously shown that HDL mediates plasminogen activator inhibitor-1 secretion in 3T3L1 adipocytes through activation of S1PR2 (16) and determined that SR-BI is also required to affect this metabolism (unpublished observation).…”

Section: Synthesis Of Recombinant Hdl and Recombinant Hdl Containing S1pmentioning

confidence: 99%

S1P in HDL promotes interaction between SR-BI and S1PR1 and activates S1PR1-mediated biological functions: calcium flux and S1PR1 internalization

Lee

Appleton

El‐Shewy

et al. 2017

Journal of Lipid Research

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Journal of Lipid Research Volume 58, 2017325 interaction between SR-BI and S1PR1 and activates S1PR1-mediated biological functions: calcium flux and S1PR1 internalization. J. Lipid Res. 2017. 58: 325-338.Supplementary key words high density lipoprotein • sphingosine 1-phosphate • protein-fragment complementation assay • scavenger receptor BI • S1P receptorsThe reverse transport of cholesterol from the periphery to the liver is often considered as the hallmark antiatherogenic function of HDL. SR-BI, the first molecularly characterized HDL receptor that plays a critical role in this metabolism, is abundantly expressed in several types of cells and tissue types, including the liver parenchyma, adrenal cortical cells, platelets, endothelial cells, smooth muscle cells, and macrophages. SR-BI facilitates the selective uptake of HDL cholesterol by cells, primarily in the form of cholesteryl esters. SR-BI also mediates the bidirectional flux of unesterified cholesterol and phospholipids between HDL and cells, which leads to an increase in cellular cholesterol mass and alters cholesterol distribution in plasma membrane domains (1-4).Numerous studies have detailed the various signaling pathways generated by the interaction of HDL with cell surface receptors that have been shown to induce myriad Abstract HDL normally transports about 50-70% of plasma sphingosine 1-phosphate (S1P), and the S1P in HDL reportedly mediates several HDL-associated biological effects and signaling pathways. The HDL receptor, SR-BI, as well as the cell surface receptors for S1P (S1PRs) may be involved partially and/or completely in these HDL-induced processes. Here we investigate the nature of the HDLstimulated interaction between the HDL receptor, SR-BI, and S1PR1 using a protein-fragment complementation assay and confocal microscopy. In both primary rat aortic vascular smooth muscle cells and HEK293 cells, the S1P content in HDL particles increased intracellular calcium concentration, which was mediated by S1PR1. Mechanistic studies performed in HEK293 cells showed that incubation of cells with HDL led to an increase in the physical interaction between the SR-BI and S1PR1 receptors that mainly occurred on the plasma membrane. Model recombinant HDL (rHDL) particles formed in vitro with S1P incorporated into the particle initiated the internalization of S1PR1, whereas rHDL without supplemented S1P did not, suggesting that S1P transported in HDL can selectively activate S1PR1. In conclusion, these data suggest that S1P in HDL stimulates the transient interaction between SR-BI and S1PRs that can activate S1PRs and induce an elevation in intracellular calcium concentration.-Lee,

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“…NO, in the modest physiological concentrations produced by eNOS, is well known to exert anti-atherosclerotic, antithrombotic, vasodilatory, and antihypertrophic effects crucial for preserving healthful structure and function of the vascular system (Cooke 2004;Massion and Balligand 2007). Recent studies show that the activation of eNOS induced by HDL and by adiponectin in endothelial cells-thought to play a key role in the vascular protection afforded by these agents-is mediated via activation of AMPK (Kimura et al 2010;Drew et al 2004;Deng et al 2010). Likewise, the ability of exerciseinduced shear stress to stimulate eNOS and boost its expression is mediated in part via AMPK; the impact on eNOS expression requires AMPK-mediated induction of the transcription factor kruppel-like factor 2 (Zhang et al 2006;Young et al 2009).…”

Section: Vascular Protectionmentioning

confidence: 99%

“…Many of these agents boost the (AMP+ADP)/ATP ratio by impeding the efficiency of mitochondrial electron transport (metformin, berberine, thiazolidinediones, dinitrophenol), inhibiting mitochondrial ATP synthase (resveratrol, quercetin) or inhibiting glycolysis (2-deoxyglucose) (Hawley et al 2010). Hormones and drugs which increase intracellular free calcium can also function as AMPK activators; for example, the ability of HDL particles to activate AMPK in endothelial cells reflects, in part, an increase in calcium influx that activates CaMKK (Kimura et al 2010). The compound 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) is converted intracellularly to an analog of AMP which mimics AMP's activating impact on AMPK.…”

Section: Ampk-cellular Monitor Of Fuel Availabilitymentioning

confidence: 99%

AMPK activation—protean potential for boosting healthspan

McCarty

2013

AGE

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AMP-activated kinase (AMPK) is activated when the cellular (AMP+ADP)/ATP ratio rises; it therefore serves as a detector of cellular "fuel deficiency." AMPK activation is suspected to mediate some of the health-protective effects of long-term calorie restriction. Several drugs and nutraceuticals which slightly and safely impede the efficiency of mitochondrial ATP g e n e r a t i o n -m o s t n o t a b l y m e t f o r m i n a n d berberine-can be employed as clinical AMPK activators and, hence, may have potential as calorie restriction mimetics for extending healthspan. Indeed, current evidence indicates that AMPK activators may reduce risk for atherosclerosis, heart attack, and stroke; help to prevent ventricular hypertrophy and manage congestive failure; ameliorate metabolic syndrome, reduce risk for type 2 diabetes, and aid glycemic control in diabetics; reduce risk for weight gain; decrease risk for a number of common cancers while improving prognosis in cancer therapy; decrease risk for dementia and possibly other neurodegenerative disorders; help to preserve the proper structure of bone and cartilage; and possibly aid in the prevention and control of autoimmunity. While metformin and berberine appear to have the greatest utility as clinical AMPK activators-as reflected by their efficacy in diabetes management-regular ingestion of vinegar, as well as moderate alcohol consumption, may also achieve a modest degree of healthprotective AMPK activation. The activation of AMPK achievable with any of these measures may be potentiated by clinical doses of the drug salicylate, which can bind to AMPK and activate it allosterically.

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Mechanism and Role of High Density Lipoprotein-induced Activation of AMP-activated Protein Kinase in Endothelial Cells

Cited by 70 publications

References 54 publications

Regulation of signal transduction by HDL

Regulation of signal transduction by HDL

S1P in HDL promotes interaction between SR-BI and S1PR1 and activates S1PR1-mediated biological functions: calcium flux and S1PR1 internalization

AMPK activation—protean potential for boosting healthspan

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