Serum prostacyclin stabilizing factor is identical to apolipoprotein A-I (Apo A-I). A novel function of Apo A-I.

Yui, Yoshiki; Aoyama, Takeshi; Morishita, Hiroshi; Takahashi, Masaki; Takatsu, Yoshiki; Kawai, Chuichi

doi:10.1172/jci113682

Cited by 190 publications

(66 citation statements)

References 26 publications

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“…Possible explanations include the fact that HDL-C has antioxidant and antiinflammatory properties (6, 7), attenuates endothelial dysfunction (8,9), has anticoagulant effects (10,11), and enhances the half-life of prostacyclin (12)(13)(14). The antiinflammatory properties of HDL-C may be particularly relevant here, because we observed systemic inflammation and endothelial activation in patients with PAH with low HDL-C levels (Table 8).…”

Section: Discussionmentioning

confidence: 84%

“…High-density lipoprotein cholesterol (HDL-C) is associated with a lower risk of coronary heart disease (4,5).The underlying mechanisms behind this protective effect include stimulation of reverse cholesterol transport, antioxidant and antiinflammatory properties (6,7), attenuation of endothelial dysfunction (8,9), anticoagulant effects (10,11), and enhancement of prostacyclin half-life (12)(13)(14). Interestingly, except for reverse cholesterol transport, derangements in all of these mechanisms have been implicated in the pathobiology of PAH.…”

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confidence: 99%

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Plasma Levels of High-Density Lipoprotein Cholesterol and Outcomes in Pulmonary Arterial Hypertension

Heresi¹,

Aytekin²,

Newman³

et al. 2010

Am J Respir Crit Care Med

114

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Rationale: High-density lipoprotein cholesterol (HDL-C) promotes healthy vascular function, and it is decreased in insulin resistance. Insulin resistance predisposes to pulmonary vascular disease. Objectives: We hypothesized that HDL-C is associated with clinical outcomes in pulmonary arterial hypertension (PAH). Methods: Plasma HDL-C concentrations were measured in 69 patients with PAH (age, 46.7 6 12.9 yr; female, 90%) and 229 control subjects (age, 57 6 13 yr; female, 48%). Clinical outcomes of interest included hospitalization for PAH, lung transplantation, and all-cause mortality. Survival and time to clinical worsening curves were derived by the Kaplan-Meier method. Cox regression modeling of outcome versus HDL-C with individual covariate adjustments was performed. Measurement and Main Results: HDL-C was low in subjects with PAH compared with control subjects (median, interquartile range: PAH: 36, 29-40 mg/dl; control subjects: 49, 40-60 mg/dl; P , 0.001). An HDL-C level of 35 mg/dl discriminated survivors from nonsurvivors, with a sensitivity of 100% and specificity of 60%. After a median follow-up of 592 days, high HDL-C was associated with decreased mortality (hazard ratio for every 5-mg/dl increase in HDL-C, 0.643; 95% confidence interval, 0.504-0.822; P 5 0.001) and less clinical worsening (hazard ratio for every 5-mg/dl increase in HDL-C, 0.798; 95% confidence interval, 0.663-0.960; P 5 0.02). HDL-C remained a significant predictor of survival after adjusting for cardiovascular risk factors, C-reactive protein, indices of insulin resistance, and severity of PAH (all P , 0.05). Conclusions: Low plasma HDL-C is associated with higher mortality and clinical worsening in PAH. This association does not appear to be explained by underlying cardiovascular risk factors, insulin resistance, or the severity of PAH.

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Section: Discussionmentioning

confidence: 84%

mentioning

confidence: 99%

Plasma Levels of High-Density Lipoprotein Cholesterol and Outcomes in Pulmonary Arterial Hypertension

Heresi¹,

Aytekin²,

Newman³

et al. 2010

Am J Respir Crit Care Med

114

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“…It also promotes an increased hydrolysis of cholesterol esters in smooth muscle cells, allowing the release of cholesterol to HDL-A1. Experiments have shown [116] that HDL-A1 prolongs the half-life of PGI2 from 5 minutes to 22 minutes. These authors showed that apo-A1 bound to HDL forms a complex with PGI2, thus delaying its degradation, and therefore promoting vasodilation and platelet stability.…”

Section: A Proposed Role For the Atheromamentioning

confidence: 99%

Is Endothelial Nitric Oxide Synthase a Moonlighting Protein Whose Day Job is Cholesterol Sulfate Synthesis? Implications for Cholesterol Transport, Diabetes and Cardiovascular Disease

Seneff

Lauritzen

Davidson³

et al. 2012

Entropy

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Theoretical inferences, based on biophysical, biochemical, and biosemiotic considerations, are related here to the pathogenesis of cardiovascular disease, diabetes, and other degenerative conditions. We suggest that the "daytime" job of endothelial nitric oxide synthase (eNOS), when sunlight is available, is to catalyze sulfate production. There is a striking alignment between cell types that produce either cholesterol sulfate or sulfated polysaccharides and those that contain eNOS. The signaling gas, nitric oxide, a wellknown product of eNOS, produces pathological effects not shared by hydrogen sulfide, a sulfur-based signaling gas. We propose that sulfate plays an essential role in HDL-A1 cholesterol trafficking and in sulfation of heparan sulfate proteoglycans (HSPGs), both critical to lysosomal recycling (or disposal) of cellular debris. HSPGs are also crucial in glucose metabolism, protecting against diabetes, and in maintaining blood colloidal suspension and capillary flow, through systems dependent on water-structuring properties of sulfate, an anionic kosmotrope. When sunlight exposure is insufficient, lipids accumulate in the atheroma in order to supply cholesterol and sulfate to the heart, using a OPEN ACCESSEntropy 2012, 14 2493 process that depends upon inflammation. The inevitable conclusion is that dietary sulfur and adequate sunlight can help prevent heart disease, diabetes, and other disease conditions.

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“…Because of its alpha-helix structure it can bind to PGI2 which is originally an unstable substance and causes PGI2 stabilization thereby imparting an important protective anti-aggregatory effect against platelet thrombi formation at sites of vascular damage. Thus it contributes towards its novel anti atherogenic function of prevention of coronary artery disease [3].…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein A-I: A Molecule of Diverse Function

2015

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Serum prostacyclin stabilizing factor is identical to apolipoprotein A-I (Apo A-I). A novel function of Apo A-I.

Cited by 190 publications

References 26 publications

Plasma Levels of High-Density Lipoprotein Cholesterol and Outcomes in Pulmonary Arterial Hypertension

Plasma Levels of High-Density Lipoprotein Cholesterol and Outcomes in Pulmonary Arterial Hypertension

Is Endothelial Nitric Oxide Synthase a Moonlighting Protein Whose Day Job is Cholesterol Sulfate Synthesis? Implications for Cholesterol Transport, Diabetes and Cardiovascular Disease

Apolipoprotein A-I: A Molecule of Diverse Function

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