Angiotensin II–induced oxidative burst is fluvastatin sensitive in neutrophils of patients with hypercholesterolemia

Serés, I.; Fóris, Gabriella; Páll, Dénes; Kosztáczky, Béla; Paragh, György; Varga, Zsuzsa

doi:10.1016/j.metabol.2005.03.021

Cited by 14 publications

(13 citation statements)

References 34 publications

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“…A recent clinical study suggested that atorvastatin (80 mg/day) caused a nonsignificant decrease in serum LTB 4 levels [28]. It has been reported that fluvastatin blocked the production of LTC 4 [29]. In accordance with the previous results, our data showed atorvastatin significantly downregulated the level of serum LTD 4 .…”

Section: Discussionsupporting

confidence: 92%

Atorvastatin Reduces Plaque Vulnerability in an Atherosclerotic Rabbit Model by Altering the 5-Lipoxygenase Pathway

et al. 2010

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Objective: The 5-lipoxygenase catalyzed formation of leukotriene lipid mediators is a mediator for inflammatory response in arteries. The present study investigated the relationship between atorvastatin and the 5-lipoxygenase pathway in an atherosclerotic rabbit model. Methods: Thirty male New Zealand White Rabbits were randomized into negative control, positive control and atorvastatin groups. At week 4, the rabbits were subjected to carotid balloon-dilation injury or carotid balloon-dilation injury, followed by treatment with atorvastatin. At week 12, all the animals were sacrificed. Plasma lipids, LTD₄, and 15-epi-lipoxin A₄ were measured using the enzymatic endpoint method and ELISA, respectively. RT-PCR was performed to detect the gene expression of 5-lipoxygenase-activating protein and cysLT1R in rabbit carotid arteries. Finally, histological analysis was used to evaluate the pathophysiological changes of rabbit carotid arteries. Results: The results showed atorvastatin markedly lowered serum lipids and LTD₄ levels compared with the control group. Similarly, mRNA expression of 5-lipoxygenase-activating protein and cysLT1R was significantly inhibited by atorvastatin. Decreased carotid plaque instability was evident in atorvastatin-treated animals, as demonstrated by a thickened elastic layer, less neointima hyperplasia and macrophage proliferation. Conclusions: Atorvastatin may stabilize carotid plaque by regulating the 5-lipoxygenase pathway in atherosclerotic rabbits and delay the progression of atherosclerosis by exerting anti-inflammatory effects.

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Section: Discussionsupporting

confidence: 92%

Atorvastatin Reduces Plaque Vulnerability in an Atherosclerotic Rabbit Model by Altering the 5-Lipoxygenase Pathway

et al. 2010

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“…These levels are similar to the concentrations we measured in neutrophils obtained from hypercholesterolemic (HC) patients (plasma cholesterol >300 mg/dL), which we found to be 73% higher than concentrations found in normal subjects (2.26±0.09 nmol/10 6 cells in HC patients, N=4, compared to 1.31±0.23 nmol/10 6 , N=5; p <0.01). Seres et al have previously reported an 89% increase in cholesterol concentration in neutrophils from HC patients (28). …”

Section: Resultsmentioning

confidence: 92%

“…Typically, cholesterol will reduce “membrane fluidity”(28, 32), but molecular membrane fluidity is not predictive of translational diffusivity measured by FRAP. In contrast, others have shown an increase in fluidity with cholesterol loading(8, 33, 34).…”

Section: Discussionmentioning

confidence: 99%

Membrane Cholesterol Is a Biomechanical Regulator of Neutrophil Adhesion

Mohler

Tian

et al. 2009

ATVB

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Objective-To evaluate the role of membrane cholesterol on human neutrophil and HL-60 biomechanics, capture, rolling, and arrest to P-selectin or IL-1-activated endothelium.Methods and Results-Methyl-β-cyclodextrin (MβCD) removed up to 73% and 45% of membrane cholesterol from HL-60 cells and neutrophils, while MβCD/cholesterol complexes resulted in maximum enrichment of 65% and 40%, respectively, above control levels. Cells were perfused at a venous wall shear rate of 100 s −1 over adherent P-selectin-coated 1-µm diameter beads, uncoated 10-µm diameter beads, P-selectin-coated surfaces, or activated endothelium. Elevated cholesterol enhanced capture efficiency to 1-µm beads and increased membrane tether growth rate by 1.5-to 2-fold, whereas cholesterol depletion greatly reduced tether formation. Elevated cholesterol levels increased tether lifetime by 17% in neutrophils and adhesion lifetime by 63% in HL-60 cells. Deformation of cholesterol-enriched neutrophils increased the contact time with 10-µm beads by 32% and the contact area by 7-fold. On both P-selectin surfaces and endothelial-cell monolayers, cholesterol-enriched neutrophils rolled more slowly, more stably, and were more likely to firmly arrest. Cholesterol depletion resulted in opposite effects.Conclusions-Increasing membrane cholesterol enhanced membrane tether formation and whole cell deformability, contributing to slower, more stable rolling on P-selectin and increased firm arrest on activated endothelium.

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“…In our patients burdened by major CRF and poly-treated, the greater prevalence of obesity in OSA group did not result in increased cytokine cellular production from both PBMCs and PMNs or in increased serum levels of the investigated cytokines. Since it has been reported that pro-inflammatory changes in various cell types are affected by the risk profile of the subjects [16][17][18][19][20][21][22][23][24] it is likely that these CRF may constitute major confounding issues in studies associating OSA with inflammation. Moreover, it has been reported that drugs used in counteracting major CRF such as statins, calcium-channel blockers, and angiotensin-converting enzyme inhibitors can reduce the upregulated pro-inflammatory cellular responses [16][17][18][21][22][23][24].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, anti-hypertensive and/or metabolic therapies are associated with modulation of systemic and cellular parameters of inflammation [14][15][16][17][18][19][20][21][22][23][24]. For the presence of those potential confounding factors (i.e.…”

Section: Introductionmentioning

confidence: 99%

Cytokine production from peripheral blood mononuclear cells and polymorphonuclear leukocytes in patients studied for suspected obstructive sleep apnea

et al. 2009

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Angiotensin II–induced oxidative burst is fluvastatin sensitive in neutrophils of patients with hypercholesterolemia

Cited by 14 publications

References 34 publications

Atorvastatin Reduces Plaque Vulnerability in an Atherosclerotic Rabbit Model by Altering the 5-Lipoxygenase Pathway

Atorvastatin Reduces Plaque Vulnerability in an Atherosclerotic Rabbit Model by Altering the 5-Lipoxygenase Pathway

Membrane Cholesterol Is a Biomechanical Regulator of Neutrophil Adhesion

Cytokine production from peripheral blood mononuclear cells and polymorphonuclear leukocytes in patients studied for suspected obstructive sleep apnea

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