Increased NADPH Oxidase Activity, gp91phox Expression, and Endothelium-Dependent Vasorelaxation During Neointima Formation in Rabbits

Paravicini, Tamara M.; Gulluyan, Lerna; Dusting, Gregory J.; Drummond, Grant Raymond

doi:10.1161/01.res.0000024106.81401.95

Cited by 87 publications

(101 citation statements)

References 38 publications

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“…2-DOG has been widely used to study intracellular redox status in pulmonary arterial endothelial cell electron transport [63,64]. Although 2-DOG was not a specific NADPH inhibitor, others such as 6-amino-nicotinamide [65] to inhibit NADPH regeneration via the pentose phosphate pathway can also be toxic and nonspecific.…”

Section: Discussionmentioning

confidence: 99%

Oxidized-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine induces vascular endothelial superoxide production: Implication of NADPH oxidase

Rouhanizadeh

Hwang

Clempus

et al. 2005

Free Radical Biology and Medicine

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Modified low-density lipoprotein (LDL) induces reactive oxygen species (ROS) production by vascular cells. It is unknown if specific oxidized components in these LDL particles such as oxidized-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (ox-PAPC) can stimulate ROS production. Bovine aortic endothelial cells (BAEC) were incubated with ox-PAPC (50 μg/ml). At 4 h, ox-PAPC significantly enhanced the rate of O 2 −• production. Pretreatment of BAEC in glucose-free Dulbecco's modified Eagle's medium plus 10 mM 2-deoxyglucose (2-DOG), the latter being an antimetabolite that blocks NADPH production by the pentose shunt, significantly reduced the rate of O 2 −• production. The intensity of NAD(P)H autofluorescence decreased by 28 ± 12% in BAEC incubated with ox-PAPC compared to untreated cells, with a further decrease in the presence of 2-DOG. Ox-PAPC also increased Nox4 mRNA expression by 2.4-fold ± 0.1 while pretreatment of BAEC with the small interfering RNA (siNox4) attenuated Nox4 RNA expression. Ox-PAPC further reduced the level of glutathione while pretreatment with apocynin (100 μM) restored the GSH level (control = 22.54 ± 0.23, GSH = 18.06 ± 0.98, apocynin = 22.55 ± 0.60,.17 ± 0.36 nmol/10 6 cells). Treatment with ox-PAPC also increased MMP-2 mRNA expression accompanied by a 1.5-fold increase in MMP-2 activity. Ox-PAPC induced vascular endothelial O 2 −• production that appears to be mediated largely by NADPH oxidase activity.

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Section: Discussionmentioning

confidence: 99%

Oxidized-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine induces vascular endothelial superoxide production: Implication of NADPH oxidase

Rouhanizadeh

Hwang

Clempus

et al. 2005

Free Radical Biology and Medicine

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“…Probucol, a lipid lowering agent with antioxidant properties, inhibits neointima formation in rabbits after balloon injury through heme oxygenase-1-dependent and -independent pathways (Deng et al 2004). Neointima formation in rabbits was shown to be driven by adventitial and endothelial Nox2-derived O 2 •− in collared arteries (Paravicini et al 2002). In rats, cuff injury neointima formation was also demonstrated to be dependent on O 2 •− (Ozumi et al 2005).…”

Section: Vascular Smooth Muscle Proliferationmentioning

confidence: 97%

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

Papaharalambus

Griendling

2007

Trends in Cardiovascular Medicine

291

224

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The development of vascular disease has its origins in an initial insult to the vessel wall by biological or mechanical factors. The disruption of homeostatic mechanisms leads to alteration of the original architecture of the vessel and its biological responsiveness, contributing to acute or chronic diseases such as stroke, hypertension and atherosclerosis. Endothelial dysfunction, macrophage infiltration of the vessel wall, and proliferation and migration of smooth muscle cells all involve different types of reactive oxygen species, produced by various vessel wall components. Although basic science and animal research have clearly established the role of reactive oxygen species in the progression of vascular disease, the failure of clinical trials with antioxidant compounds has underscored the need for better antioxidant therapies and a more thorough understanding of the role of reactive oxygen species in cardiovascular physiology and pathology.The fundamental processes underlying the development of vascular diseases such as atherosclerosis, restenosis and hypertensive vascular remodeling have their origins in an initial insult to the vessel wall. Such an insult may arise from mechanical disruption that occurs during percutaneous coronary angioplasty or at regions of oscillatory shear stress, or it can result from biological causes, such as hypercholesterolemia, excess free radicals, diabetes, increased concentrations of plasma homocysteine, or infectious agents. Injury promotes disruption of the homeostatic mechanisms of the endothelial protective barrier, changing its natural properties, increasing its adhesiveness to leukocytes and altering its permeability. This endothelial dysfunction also leads to the formation of vasoactive molecules, which in turn induce inflammatory genes, inactivate nitric oxide (NO • ) and its protective functions, and activate matrix metalloproteinases, leading to extracellular matrix remodeling, and increased smooth muscle cell (VSMC) growth, migration and proliferation. Each of these processes contributes to thickening of the vessel wall or the formation of lesions that can lead to hypertension, acute myocardial infarction and stroke. Reactive Oxygen Species and Vascular InjuryIn the past decade a staggering amount of evidence implicates a common denominator, reactive oxygen species (ROS), in the development of most cardiovascular diseases (Figure 1). Superoxide (O 2 •− ) and hydrogen peroxide (H 2 O 2 ) are two of the most biologically important ROS in the cardiovascular system, and are produced in vascular cells by a number of oxidases, including the NADPH oxidases (Nox) and xanthine oxidase, lipoxygenases, cytochrome p450,

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“…20 ANP mRNA was quantified by real time PCR and the ⌬⌬Ct method with 18S ribosomal RNA as the internal standard. 20,21 Primers and probes were designed from rat-specific sequences published on GenBank (Table). Probes were 5Ј-labeled with the reporter dye FAM (ANP) or VIC (18S) and 3Ј-labeled with the quencher molecule carboxytetramethylrhodamine (TAMRA).…”

Section: Anp Mrna Expressionmentioning

confidence: 99%

“…All reactions were performed in the ABI Prism ® 7700 sequence detection system (Applied Biosystems) as described. 20 …”

Section: Anp Mrna Expressionmentioning

confidence: 99%

Acute Antihypertrophic Actions of Bradykinin in the Rat Heart

et al. 2002

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Abstract-The antihypertrophic action of angiotensin (Ang)-converting enzyme (ACE) inhibitors in the heart is attributed in part to potentiation of bradykinin. Bradykinin prevents hypertrophy of cultured cardiomyocytes by releasing nitric oxide (NO) from endothelial cells, which increases cardiomyocyte guanosine 3Ј5Ј-cyclic monophosphate (cyclic GMP). It is unknown whether cyclic GMP is essential for the action of bradykinin, or whether findings in isolated cardiomyocytes apply in whole hearts, in the presence of other cell types and mechanical/dynamic activity. We now examine the contribution of cyclic GMP to the antihypertrophic action of bradykinin in cardiomyocytes and perfused hearts. In adult rat isolated cardiomyocytes cocultured with bovine aortic endothelial cells, the inhibitory action of bradykinin (10 mol/L) against Ang II (1 mol/L)-induced 3 H]phenylalanine incorporation and atrial natriuretic peptide mRNA expression were prevented by bradykinin (100 nmol/L), the NO donor sodium nitroprusside (3 mol/L), and the ACE inhibitor ramiprilat (100 nmol/L). The acute antihypertrophic action of bradykinin was accompanied by increased left ventricular cyclic GMP, and the ramiprilat effect was attenuated by HOE 140 (1 mol/L, a B 2 -kinin receptor antagonist) or [1,2,4] oxadiazolo[4,3-a]quinoxalin-1-one (100 nmol/L). In conclusion, bradykinin exerts a direct inhibitory action against the acute hypertrophic response to Ang II in rat isolated hearts, and elevation of cardiomyocyte cyclic GMP may be an important antihypertrophic mechanism used by bradykinin and ramiprilat in the heart. Key Words: angiotensin-converting enzyme Ⅲ angiotensin II Ⅲ bradykinin Ⅲ cyclic GMP Ⅲ hypertrophy Ⅲ myocytes Ⅲ nitric oxide A ngiotensin-converting enzyme (ACE) inhibitors are often used to treat cardiac hypertrophy, 1 a significant cardiovascular risk factor in hypertensive patients. 2 The antihypertrophic action of ACE inhibitors in vivo is abolished by the B 2 -kinin receptor antagonist HOE 140, 3 indicating a significant contribution by bradykinin. In addition, B 2 -kinin receptor deficiency promotes the development of cardiac hypertrophy in vivo, 4 whereas kallikrein overexpression prevents cardiac growth. 5 However, the mechanism by which bradykinin counteracts hypertrophic stimuli in the heart is not fully understood. We have shown that bradykinin prevents hypertrophy of isolated cardiomyocytes by stimulating the release of NO from endothelial cells 6 and that this action is associated with elevation of cardiomyocyte cyclic GMP. 7 An analogue of cyclic GMP, 8-bromo-cyclic GMP, also prevents hypertrophy of isolated rat cardiomyocytes, 8 but whether stimulation of cyclic GMP is essential for the antihypertrophic action of bradykinin has not been addressed.Cardiomyocyte hypertrophy is characterized by increased protein synthesis and cell size and induction of the immediate early (eg, c-fos, c-jun, and c-myc) and fetal genes (eg, ␤-myosin heavy chain, skeletal ␣-actin, and atrial natriuretic peptide, ANP). 9 These cellular changes...

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Increased NADPH Oxidase Activity, gp91phox Expression, and Endothelium-Dependent Vasorelaxation During Neointima Formation in Rabbits

Cited by 87 publications

References 38 publications

Oxidized-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine induces vascular endothelial superoxide production: Implication of NADPH oxidase

Oxidized-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine induces vascular endothelial superoxide production: Implication of NADPH oxidase

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

Acute Antihypertrophic Actions of Bradykinin in the Rat Heart

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