The prevention of endothelial dysfunction through endothelial cell apoptosis inhibition in a hypercholesterolemic rabbit model: the effect of L-arginine supplementation

Nematbakhsh, Mehdi; Haghjooy-Javanmard, Shaghayegh; Mahmoodi, Farzaneh; Monajemi, Alireza

doi:10.1186/1476-511x-7-27

Cited by 15 publications

(9 citation statements)

References 59 publications

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“…L-arginine (a NOS substrate) depletion in animal models of atherosclerosis and hypercholesterolemia induces platelet aggregation, cell proliferation, and vascular monocyte accumulation, whereas endothelial-dependent vasoreactivity is improved in hypercholesterolemic rabbits treated with L-arginine, thus attenuating the mechanisms of vascular lesion 26 and inhibiting neointimal proliferation 27 , which can be assessed by means of several endothelial cell markers proposed (Table 1).…”

Section: Introductionmentioning

confidence: 99%

Aterosclerose experimental em coelhos

Dornas

Oliveira²,

Augusto³

et al. 2010

Arq. Bras. Cardiol.

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Section: Introductionmentioning

confidence: 99%

Aterosclerose experimental em coelhos

Dornas

Oliveira²,

Augusto³

et al. 2010

Arq. Bras. Cardiol.

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“…The apoptosis rate of smooth muscle cells in atherosclerotic lesions was shown to be 11±7.8% in miniature pigs on a high-fat diet for 37 weeks (14). Nematbakhsh et al (15) observed an endothelial cell apoptosis rate of 8% in hyperlipidemic rabbits. However, the reason for the significant difference in the apoptosis rate of nerve cells and other cells exposed to hyperlipidemia has not been determined.…”

Section: Neuronal Apoptosis Rate Is Lower Compared To That In Other Cmentioning

confidence: 99%

The dual behavior of PCSK9 in the regulation of apoptosis is crucial in Alzheimer’s disease progression (Review)

Tang

Peng

et al. 2013

Biomedical Reports

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Abstract. Neuronal apoptosis is crucial in neurodegenerative diseases. However, a lower apoptotic rate of nerve cells is detected in the brain compared to that in other organs in neurodegenerative patients or in animal models, suggesting that neuronal apoptosis induced by any type of risk factors is intricately regulated. Human and animal studies demonstrated that a high concentration of oxidized LDL (ox-LDL) in the brain, which is associated with hyperlipidemia, is one of the key apoptosis inducers in neurodegenerative diseases. However, the mechanism underlying the ox-LDL-mediated regulation of neuronal apoptosis has not been fully elucidated. Recently, we investigated proprotein convertase subtilisin̸kexin type 9 (PCSK9), a striking gene involved in lipid metabolism that exhibits a positive correlation with macrophage and endothelial cell apoptosis induced by ox-LDL. Moreover, PCSK9 may degrade β-site amyloid precursor protein-cleaving enzyme 1 (BACE1), the key enzyme cleaving amyloid precursor protein (APP) to generate amyloid β peptide (Aβ). Aβ is another key apoptosis inducer in neurodegenerative diseases. Our findings indicated that PCSK9 may be upregulated by the high levels of ox-LDL in the brain associated with hyperlipidemia and promote neuronal apoptosis through the NF-κB-B-cell lymphoma 2 (Bcl-2)/Bax-caspase 9-caspase 3 signaling pathways. Moreover, increased PCSK9 levels may inhibit the APP̸Aβ metabolic pathway and reduce Aβ generation by degrading BACE1, thereby decreasing Aβ-induced neuronal apoptosis. The dual regulation mechanism of PCSK9 on apoptosis maintains neuronal apoptosis induced by risk factors at low levels.

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“…Recently, it was demonstrated that exogenous in vivo NO treatment using nitratethiol, nitrosothiol or nitroglycerine protects SMCs against apoptosis and drives cells to quiescence through up‐regulation of p53 and increased levels of Bcl‐2/Bax (Duran et al ., 2009). Moreover, endothelial cell apoptosis was inhibited in rabbit lesions if the animals received L‐arginine, an essential substance for nitric oxide synthesis (Nematbakhsh et al ., 2008). Interestingly, treatment of plaques in cholesterol‐fed rabbits with the NO donor molsidomine leads to the formation of a large subendothelial macrophage‐free layer solely consisting of SMCs and extracellular matrix (De Meyer et al ., 2003).…”

Section: Pharmacological Stimulation Of Cell Death In Atherosclerosismentioning

confidence: 99%

Pharmacological modulation of cell death in atherosclerosis: a promising approach towards plaque stabilization?

Martinet¹,

Schrijvers

Meyer

2011

British Journal of Pharmacology

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Despite tremendous advances over the last 15 years in identifying vulnerable atherosclerotic plaques, the incidence of death and disability caused by such lesions still remains the number one health threat in developed countries. Therefore, new systemic or focal therapies aimed at decreasing the overall burden of disease, and a change to a more benign phenotype, are needed. Because cell death is a prominent feature of advanced atherosclerotic plaques with a major impact on plaque destabilization, an increasing number of compounds targeting the apoptotic or autophagic machinery in atherosclerosis are being explored, predominantly at the preclinical level. This review will provide an overview of these compounds, with a focus on both inhibition and stimulation of cell death, to prevent acute coronary syndromes and sudden cardiac death. AbbreviationsCHOP, C/EBP homologous protein; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; ER, endoplasmic reticulum; FA, fatty acids; FasL, Fas ligand; FLIP, FLICE inhibitory protein; HDL, high-density lipoprotein; IL-1ra, interleukin-1 receptor antagonist; iNOS, inducible nitric oxide synthase; LDL, low-density lipoprotein; LOX-1, lectin-like oxidized low density lipoprotein receptor-1; LXR, liver X receptor; MCP-1, monocyte chemotactic protein-1; mTOR, mammalian target of rapamycin; NO, nitric oxide; oxLDL, oxidized low-density lipoprotein; PBA, 4-phenyl butyric acid; RIP1, receptor-interacting protein 1; ROS, reactive oxygen species; SCD-1, stearoyl-Coenzyme A desaturase-1; SMC, smooth muscle cell; TUDCA, tauroursodeoxycholic acid; TZD, thiazolidinedione; UPR, unfolded protein response; VCAM-1, vascular cell adhesion molecule-1

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The prevention of endothelial dysfunction through endothelial cell apoptosis inhibition in a hypercholesterolemic rabbit model: the effect of L-arginine supplementation

Cited by 15 publications

References 59 publications

Aterosclerose experimental em coelhos

Aterosclerose experimental em coelhos

The dual behavior of PCSK9 in the regulation of apoptosis is crucial in Alzheimer’s disease progression (Review)

Pharmacological modulation of cell death in atherosclerosis: a promising approach towards plaque stabilization?

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