HDL levels and oxidizability during myocardial infarction are associated with reduced endothelial-mediated vasodilation and nitric oxide bioavailability

Carvalho, Luiz Sérgio F.; Panzoldo, Natália Baratella; Santos, Simone N.; Modolo, Rodrigo; Almeida, Breno Oliveira; Silva, José C. Quinaglia e; Nadruz, Wilson; Faria, Eliana Cotta de; Sposito, Andrei C.

doi:10.1016/j.atherosclerosis.2014.10.103

Cited by 23 publications

(12 citation statements)

References 28 publications

(42 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies have suggested that the endothelial effects of HDL are highly heterogeneous, and that atheroprotective effects of HDL are impaired in patients with type II diabetes mellitus, metabolic syndrome, coronary artery disease and chronic heart failure. [35][36][37][38] The present study showed that FMD was significantly smaller in subjects with extremely high HDL-C as well as subjects with low HDL-C than in subjects with high HDL-C. After adjustment for cardiovascular risk factors, extremely high HDL-C, but not low HDL-C, was significantly associated with endothelial dysfunction.…”

Section: Discussionsupporting

confidence: 46%

Association of extremely high levels of high-density lipoprotein cholesterol with endothelial dysfunction in men

Takaeko

Matsui

Kajikawa

et al. 2019

Journal of Clinical Lipidology

View full text Add to dashboard Cite

BACKGROUND: It is not clear whether a high level of high-density lipoprotein cholesterol (HDL-C) is associated with lower risk of atherosclerosis. It is likely that HDL-C is a double-edged sword for atherosclerosis. OBJECTIVE: The purpose of this study was to evaluate the relationship between HDL-C levels and endothelial function in men. METHODS: This was a cross-sectional study. We evaluated flow-mediated vasodilation (FMD) and serum levels of HDL-C in 5842 men aged 18 to 92 years who were not receiving lipid-lowering therapy. All participants were divided into four groups by HDL-C level: low HDL-C (,40 mg/dL),

show abstract

Section: Discussionsupporting

confidence: 46%

Association of extremely high levels of high-density lipoprotein cholesterol with endothelial dysfunction in men

Takaeko

Matsui

Kajikawa

et al. 2019

Journal of Clinical Lipidology

View full text Add to dashboard Cite

show abstract

“…During the acute phase of ST-segment elevation myocardial infarction (STEMI), the concentration of HDL particles is reduced, and these HDL particles are less protective against LDL oxidation and more susceptible to auto-oxidation; both of these changes are associated with a reduction in brachial artery endothelial vasomotor function 89 . Whether these HDL functional changes would remain significant after adjustment for reduced HDL particle number, however, is unknown.…”

Section: Hdl Functionality and Atherosclerosismentioning

confidence: 99%

Dysfunctional HDL and atherosclerotic cardiovascular disease

et al. 2015

View full text Add to dashboard Cite

High-density lipoproteins (HDLs) protect against atherosclerosis by removing excess cholesterol from macrophages through the ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1) pathways involved in reverse cholesterol transport. Factors that impair the availability of functional apolipoproteins or the activities of ABCA1 and ABCG1 could, therefore, strongly influence atherogenesis. HDL also inhibits lipid oxidation, restores endothelial function, exerts anti-inflammatory and antiapoptotic actions, and exerts anti-inflammatory actions in animal models. Such properties could contribute considerably to the capacity of HDL to inhibit atherosclerosis. Systemic and vascular inflammation has been proposed to convert HDL to a dysfunctional form that has impaired antiatherogenic effects. A loss of anti-inflammatory and antioxidative proteins, perhaps in combination with a gain of proinflammatory proteins, might be another important component in rendering HDL dysfunctional. The proinflammatory enzyme myeloperoxidase induces both oxidative modification and nitrosylation of specific residues on plasma and arterial apolipoprotein A-I to render HDL dysfunctional, which results in impaired ABCA1 macrophage transport, the activation of inflammatory pathways, and an increased risk of coronary artery disease. Understanding the features of dysfunctional HDL or apolipoprotein A-I in clinical practice might lead to new diagnostic and therapeutic approaches to atherosclerosis.

show abstract

“…High‐density lipoprotein (HDL) stimulates eNOS‐mediated NO production in vitro and in vivo . Moreover, in dyslipidaemic patients, the infusion of reconstituted HDL particles containing apolipoprotein A1 (APOA1) and phosphatidylcholine restores endothelium‐dependent vasodilatation by increasing NO bioavailability .…”

Section: Introductionmentioning

confidence: 99%

Pharmacological inhibition of the F₁‐ATPase/P2Y₁ pathway suppresses the effect of apolipoprotein A1 on endothelial nitric oxide synthesis and vasorelaxation

et al. 2019

View full text Add to dashboard Cite

Aim The contribution of apolipoprotein A1 (APOA1), the major apolipoprotein of high‐density lipoprotein (HDL), to endothelium‐dependent vasodilatation is unclear, and there is little information regarding endothelial receptors involved in this effect. Ecto‐F1‐ATPase is a receptor for APOA1, and its activity in endothelial cells is coupled to adenosine diphosphate (ADP)‐sensitive P2Y receptors (P2Y ADP receptors). Ecto‐F1‐ATPase is involved in APOA1–mediated cell proliferation and HDL transcytosis. Here, we investigated the effect of lipid‐free APOA1 and the involvement of ecto‐F1‐ATPase and P2Y ADP receptors on nitric oxide (NO) synthesis and the regulation of vascular tone. Method Nitric oxide synthesis was assessed in human endothelial cells from umbilical veins (HUVECs) and isolated mouse aortas. Changes in vascular tone were evaluated by isometric force measurements in isolated human umbilical and placental veins and by assessing femoral artery blood flow in conscious mice. Results Physiological concentrations of lipid‐free APOA1 enhanced endothelial NO synthesis, which was abolished by inhibitors of endothelial nitric oxide synthase (eNOS) and of the ecto‐F1‐ATPase/P2Y1 axis. Accordingly, APOA1 inhibited vasoconstriction induced by thromboxane A2 receptor agonist and increased femoral artery blood flow in mice. These effects were blunted by inhibitors of eNOS, ecto‐F1‐ATPase and P2Y1 receptor. Conclusions Using a pharmacological approach, we thus found that APOA1 promotes endothelial NO production and thereby controls vascular tone in a process that requires activation of the ecto‐F1‐ATPase/P2Y1 pathway by APOA1. Pharmacological targeting of this pathway with respect to vascular diseases should be explored.

show abstract

HDL levels and oxidizability during myocardial infarction are associated with reduced endothelial-mediated vasodilation and nitric oxide bioavailability

Cited by 23 publications

References 28 publications

Association of extremely high levels of high-density lipoprotein cholesterol with endothelial dysfunction in men

Association of extremely high levels of high-density lipoprotein cholesterol with endothelial dysfunction in men

Dysfunctional HDL and atherosclerotic cardiovascular disease

Pharmacological inhibition of the F₁‐ATPase/P2Y₁ pathway suppresses the effect of apolipoprotein A1 on endothelial nitric oxide synthesis and vasorelaxation

Contact Info

Product

Resources

About

HDL levels and oxidizability during myocardial infarction are associated with reduced endothelial-mediated vasodilation and nitric oxide bioavailability

Cited by 23 publications

References 28 publications

Association of extremely high levels of high-density lipoprotein cholesterol with endothelial dysfunction in men

Association of extremely high levels of high-density lipoprotein cholesterol with endothelial dysfunction in men

Dysfunctional HDL and atherosclerotic cardiovascular disease

Pharmacological inhibition of the F1‐ATPase/P2Y1 pathway suppresses the effect of apolipoprotein A1 on endothelial nitric oxide synthesis and vasorelaxation

Contact Info

Product

Resources

About

Pharmacological inhibition of the F₁‐ATPase/P2Y₁ pathway suppresses the effect of apolipoprotein A1 on endothelial nitric oxide synthesis and vasorelaxation