High-Density Lipoproteins Protect Endothelial Cells from Tumor Necrosis Factor-α-Induced Apoptosis

Shinoda, Masahiro; Tsuchida, Keiko; Makino, Naoki

doi:10.1006/bbrc.2000.2877

Cited by 166 publications

(118 citation statements)

References 21 publications

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“…Importantly, both the protein and lipid moieties have been reported to contribute to the antiapoptotic capacity of HDL. ApoA-I has been shown to inhibit endothelial cell apoptosis induced by oxLDL, VLDL, and TNF-α (Speidel et al 1990;Suc et al 1997;Sugano et al 2000). In a more detailed study, HDL subpopulations enriched with apoA-I account for approximately 70 % of the antiapoptotic activity of HDL in a cell culture model with human microvascular endothelial cells that were treated with mildly oxidized LDL.…”

Section: Mechanisms Under Physiological Conditionsmentioning

confidence: 97%

“…The situation is completely different in atherosclerotic plaques, in a high oxidative stress environment where macrophages produce high amounts of nitric oxide or peroxynitrite that could induce apoptotic cell death (Kockx and Herman 2000). In the aorta the capacity of HDL to quench endothelial cell apoptosis may therefore represent an antiatherogenic property of HDL (de Souza et al 2010;Nofer et al 2001;Suc et al 1997;Sugano et al 2000). HDL has been shown to attenuate endothelial cell apoptosis induced by different stimuli such as TNF-α, oxLDL, and growth factor deprivation (de Souza et al 2010;Nofer et al 2001;Suc et al 1997;Sugano et al 2000).…”

Section: Mechanisms Under Physiological Conditionsmentioning

confidence: 99%

“…In the aorta the capacity of HDL to quench endothelial cell apoptosis may therefore represent an antiatherogenic property of HDL (de Souza et al 2010;Nofer et al 2001;Suc et al 1997;Sugano et al 2000). HDL has been shown to attenuate endothelial cell apoptosis induced by different stimuli such as TNF-α, oxLDL, and growth factor deprivation (de Souza et al 2010;Nofer et al 2001;Suc et al 1997;Sugano et al 2000). It has been suggested that HDL may inhibit both death-receptor and mitochondrial-mediated apoptotic pathways.…”

Section: Mechanisms Under Physiological Conditionsmentioning

confidence: 99%

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Dysfunctional HDL: From Structure-Function-Relationships to Biomarkers

Riwanto

Rohrer

Eckardstein

et al. 2014

Handbook of Experimental Pharmacology

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Reduced plasma levels of HDL-C are associated with an increased risk of CAD and myocardial infarction, as shown in various prospective population studies. However, recent clinical trials on lipidmodifying drugs that increase plasma levels of HDL-C have not shown significant clinical benefit. Notably, in some recent clinical studies, there is no clear association of higher HDL-C levels with a reduced risk of cardiovascular events observed in patients with existing CAD. These observations have prompted researchers to shift from a cholesterol-centric view of HDL towards assessing the function and composition of HDL particles. Of importance, experimental and translational studies have further demonstrated various potential antiatherogenic effects of HDL. HDL has been proposed to promote macrophage reverse cholesterol transport and to protect endothelial cell functions by prevention of oxidation of LDL and its adverse endothelial effects. Furthermore, HDL from healthy subjects can directly stimulate endothelial cell production of nitric oxide and exert anti-inflammatory and antiapoptotic effects. Of note, increasing evidence suggests that the vascular effects of HDL can be highly heterogeneous and HDL may lose important anti-atherosclerotic properties and turn dysfunctional in patients with chronic inflammatory disorders. A greater understanding of mechanisms of action of HDL and its altered vascular effects is therefore critical within the context of HDL-targeted therapies.

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Section: Mechanisms Under Physiological Conditionsmentioning

confidence: 97%

Section: Mechanisms Under Physiological Conditionsmentioning

confidence: 99%

Section: Mechanisms Under Physiological Conditionsmentioning

confidence: 99%

See 1 more Smart Citation

Dysfunctional HDL: From Structure-Function-Relationships to Biomarkers

Riwanto

Rohrer

Eckardstein

et al. 2014

Handbook of Experimental Pharmacology

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“…Oxidative stress and inflammation are common features of CKD and promote endothelial cell injury and apoptosis. Acting via its constituent ApoA-1 and sphingosine-1 phosphate (S1P) proteins, HDL lowers caspase-3 activity, inhibits the formation of ROS, and prevents apoptosis of endothelial cells [22][23][24] . In addition, normal HDL facilitates the repair, migration, and proliferation of endothelial cells and increases the number of circulating endothelial progenitor cells -events that are essential for vascular repair and prevention of plaque formation [25][26][27] ( FIG.…”

Section: Biologic Functions Of Normal Hdlmentioning

confidence: 99%

HDL abnormalities in nephrotic syndrome and chronic kidney disease

2015

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| Normal HDL activity confers cardiovascular and overall protection by mediating reverse cholesterol transport and through its potent anti-inflammatory, antioxidant, and antithrombotic functions. Serum lipid profile, as well as various aspects of HDL metabolism, structure, and function can be profoundly altered in patients with nephrotic range proteinuria or chronic kidney disease (CKD). These abnormalities can, in turn, contribute to the progression of cardiovascular complications and various other comorbidities, such as foam cell formation, atherosclerosis, and/or glomerulosclerosis, in affected patients. The presence and severity of proteinuria and renal insufficiency, as well as dietary and drug regimens, pre-existing genetic disorders of lipid metabolism, and renal replacement therapies (including haemodialysis, peritoneal dialysis, and renal transplantation) determine the natural history of lipid disorders in patients with kidney disease. Despite the adverse effects associated with dysregulated reverse cholesterol transport and advances in our understanding of the underlying mechanisms, safe and effective therapeutic interventions are currently lacking. This Review provides an overview of HDL metabolism under normal conditions, and discusses the features, mechanisms, and consequences of HDL abnormalities in patients with nephrotic syndrome or advanced CKD.

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“…The result of current research suggested that the abnormal metabolism of blood lipids, including a reduced level of HDL-C and an elevated level of TG, affected the functions of vascular endothelium and increased the activity of platelets 9,10 resulting in abnormal coagulatory functions and promoting inflammatory responses. [11][12][13] High-density lipoprotein inhibited the apoptosis of endothelial cells through the regulation of their proliferation 14,15 so as to maintain their structural integrity. In the meantime, HDL could boost the production of eNOS in endothelial cells so as to further increase the release of nitric oxide (NO) and enhance the bioavailability of NO.…”

Section: Discussionmentioning

confidence: 99%

Correlation Study of Pulmonary Embolism and High‐density Lipoprotein Cholesterol

Wang

2010

Clinical Cardiology

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Background: It is currently thought that pulmonary embolism and deep vein thrombosis are different manifestations of the same pathological process of venous thromboembolism. Venous thromboembolism has a negative correlation with high-density lipoprotein cholesterol. Hypothesis: Pulmonary embolism has a negative correlation with the level of high-density lipoprotein cholesterol. Methods: A total of 90 patients with pulmonary embolism, diagnosed and treated at a single center, were retrospectively analyzed for the present study. Among them were 57 cases of pulmonary arterial trunk embolism in group A and 33 cases of pulmonary arterial non-trunk embolism in group B.Results: The results showed that the level of high-density lipoprotein cholesterol decreased markedly in patients with pulmonary arterial trunk embolism as compared to those with pulmonary arterial non-trunk embolism. A stepwise logistic regression analysis was performed upon the relationship between pulmonary arterial trunk embolism and multiple factors. The results showed that a pulmonary arterial trunk embolism had a negative correlation with the level of high-density lipoprotein cholesterol and a positive correlation with triglyceride and high sensitivity C-reactive protein.Conclusions: Pulmonary arterial trunk embolism is negatively correlated with the level of high-density lipoprotein cholesterol.

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High-Density Lipoproteins Protect Endothelial Cells from Tumor Necrosis Factor-α-Induced Apoptosis

Cited by 166 publications

References 21 publications

Dysfunctional HDL: From Structure-Function-Relationships to Biomarkers

Dysfunctional HDL: From Structure-Function-Relationships to Biomarkers

HDL abnormalities in nephrotic syndrome and chronic kidney disease

Correlation Study of Pulmonary Embolism and High‐density Lipoprotein Cholesterol

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