Lipid-Free Apolipoprotein A-I and Discoidal Reconstituted High-Density Lipoproteins Differentially Inhibit Glucose-Induced Oxidative Stress in Human Macrophages

Tabet, Fatiha; Lambert, Gilles; Torres, Luisa; Hou, Liming; Sotirchos, Irene M.; Touyz, Rhian M.; Jenkins, Alicia J.; Barter, Philip J.; Rye, Kerry‐Anne

doi:10.1161/atvbaha.110.222000

Cited by 36 publications

(23 citation statements)

References 48 publications

(41 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…BR also inhibited the TNF-α-mediated nuclear translocation of the NF-κB p65 subunit (Online Figure IIIB) and reduced the TNF-α-mediated increase in intracellular GSSG levels (Online Figure IIIC; P<0.05 for all). These effects of BR are consistent with what we have reported previously for the inhibition of TNF-α-induced activation of NF-κB 5 and oxidative stress 24 by (A-I)rHDL.…”

Section: The Ho-1 Metabolic Product Br Mimics the Anti-inflammatorysupporting

confidence: 92%

High-Density Lipoproteins Inhibit Vascular Endothelial Inflammation by Increasing 3β-Hydroxysteroid-Δ24 Reductase Expression and Inducing Heme Oxygenase-1

Chen

Shrestha

et al. 2013

Circulation Research

Self Cite

View full text Add to dashboard Cite

Rationale: Lipid-free apolipoprotein (apo) A-I and discoidal reconstituted high-density lipoproteins (rHDL) containing apoA-I, (A-I)rHDL, inhibit vascular inflammation by increasing 3β-hydroxysteroid-Δ24 reductase (DHCR24) expression. Objective: To determine whether the lipid-free apoA-I–mediated and (A-I)rHDL-mediated increase in DHCR24 expression induces the cytoprotective and potentially cardioprotective enzyme, heme oxygenase-1 (HO-1). Methods and Results: In vivo: A single intravenous infusion of lipid-free apoA-I (8 mg/kg) administered 24 hours before inserting a nonocclusive periarterial carotid collar into New Zealand White rabbits decreased collar-induced endothelial vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression, reduced intima/media neutrophil infiltration, and increased DHCR24 and HO-1 mRNA levels. Knockdown of vascular DHCR24 and HO-1 and systemic administration of tin-protoporphyrin-IX, an HO inhibitor, abolished these anti-inflammatory effects. In vitro: Preincubation of human coronary artery endothelial cells with (A-I)rHDL before activation with tumor necrosis factor-α increased DHCR24 and HO-1 mRNA levels and inhibited cytokine-induced vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression. Transfection of the cells with DHCR24 and HO-1 small interfering RNA and tin-protoporphyrin-IX treatment abolished these effects. The (A-I)rHDL-mediated induction of HO-1 was reduced in human coronary artery endothelial cells transfected with DHCR24 small interfering RNA. Transfection of human coronary artery endothelial cells with HO-1 small interfering RNA and tin-protoporphyrin-IX treatment did not inhibit the (A-I)rHDL-mediated increase in DHCR24 expression. Inhibition of phosphatidylinositol 3-kinase/Akt reduced the (A-I)rHDL-mediated increase in HO-1, but not DHCR24 expression. The activation of phosphatidylinositol 3-kinase/Akt by (A-I)rHDL was decreased in human coronary artery endothelial cells that were transfected with DHCR24 small interfering RNA. Conclusions: Lipid-free apoA-I and (A-I)rHDL inhibit inflammation by increasing DHCR24 expression, which, in turn, activates phosphatidylinositol 3-kinase/Akt and induces HO-1.

show abstract

Section: The Ho-1 Metabolic Product Br Mimics the Anti-inflammatorysupporting

confidence: 92%

High-Density Lipoproteins Inhibit Vascular Endothelial Inflammation by Increasing 3β-Hydroxysteroid-Δ24 Reductase Expression and Inducing Heme Oxygenase-1

Chen

Shrestha

et al. 2013

Circulation Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…The former studies further (JAK2) activation of STAT3 diminish the induction of infl ammatory cytokines by LPS ( 76 ). Lipid-free apoA-I, reconstituted HDL, and native HDL also inhibit highglucose-induced redox signaling in macrophages, with lipid-free apoA-I doing so through ABCG1-dependent increases in superoxide dismutase 1 and superoxide dismutase 2, and an attenuation in Nox2 expression ( 77 ). In neutrophils, native HDL and apoA-I decrease the surface expression of CD11b.…”

Section: Endothelial Cellsmentioning

confidence: 90%

Regulation of signal transduction by HDL

Mineo

Shaul

2013

Journal of Lipid Research

View full text Add to dashboard Cite

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.

show abstract

“…Lipid-free Apo-AI and reconstituted HDL were both shown to inhibit glucose-induced oxidative stress in macrophages by inhibiting Nox2 protein expression on one hand, while increasing superoxide dismutase expression on the other. These effects are mediated by the same cellular receptors that induce cholesterol efflux: ABCA-1 and SR-BI, thus forming another connection between HDL antioxidative activity and reverse cholesterol transport activity [20]. …”

Section: Hdl Functionmentioning

confidence: 99%

HDL dysfunction in diabetes: causes and possible treatments

Farbstein¹,

Levy

2012

Expert Review of Cardiovascular Therapy

138

105

View full text Add to dashboard Cite

HDL is known to be inversely correlated with cardiovascular disease due to its diverse antiatherogenic functions. These functions include cholesterol efflux and reverse cholesterol transport, antioxidative and anti-inflammatory activities. However, HDL has been shown to undergo a loss of function in several pathophysiological states, as in the acute phase response, obesity and chronic inflammatory diseases. Some of these diseases were also shown to be associated with increased risk for cardiovascular disease. One such disease that is associated with HDL dysfunction and accelerated atherosclerosis is diabetes mellitus, a disease in which the HDL particle undergoes diverse structural modifications that result in significant changes in its function. This review will summarize the changes that occur in HDL in diabetes mellitus and how these changes lead to HDL dysfunction. Possible treatments for HDL dysfunction are also briefly described.

show abstract

Lipid-Free Apolipoprotein A-I and Discoidal Reconstituted High-Density Lipoproteins Differentially Inhibit Glucose-Induced Oxidative Stress in Human Macrophages

Cited by 36 publications

References 48 publications

High-Density Lipoproteins Inhibit Vascular Endothelial Inflammation by Increasing 3β-Hydroxysteroid-Δ24 Reductase Expression and Inducing Heme Oxygenase-1

High-Density Lipoproteins Inhibit Vascular Endothelial Inflammation by Increasing 3β-Hydroxysteroid-Δ24 Reductase Expression and Inducing Heme Oxygenase-1

Regulation of signal transduction by HDL

HDL dysfunction in diabetes: causes and possible treatments

Contact Info

Product

Resources

About