Brief Review |
From the Division of Cardiology, Emory University, Atlanta, Ga.
Correspondence to Kathy K. Griendling, PhD, Division of Cardiology, Emory University School of Medicine, 1639 Pierce Dr, 319 WMB, Atlanta, GA 30322. E-mail kgriend{at}emory.edu
| Abstract |
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Key Words: reactive oxygen species vascular smooth muscle endothelial cells hypertension atherosclerosis
| Introduction |
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| Production and Metabolism of ROS |
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, and interleukin (IL)-1ß, thus profoundly
affecting ROS levels.8 9 10 11 The tight regulation of both
production and removal of ROS makes fluctuations in their
levels transient, another requirement for second messengers. ROS may
also act as an intracellular "rheostat," closely modulating the
activity of a discrete set of biochemical reactions. A schematic of the
balance between oxidative and reductive states of the cell and the
hormones, enzymes, and compounds that can alter this balance and thus,
the overall response of the cell, is presented in Figure 1
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Vascular NAD(P)H Oxidases
The major sources of ROS in the vessel wall, the vascular NAD(P)H
oxidases, are similar in structure to the neutrophil NADPH oxidase,
which consists of 4 major subunits: a cytochrome b558,
comprising gp91phox and p22phox, and 2 cytosolic components, p47phox
and p67phox. A member of the low-molecular-weight G protein rac family
participates in the assembly of the active complex. Table 1
summarizes the expression of the major
phox subunits in vascular cells. Although the expression pattern of
these molecules has been demonstrated, with the exception of p22phox in
vascular smooth muscle cells (VSMCs)12 and
endothelial cells13 and rac15
and p67phox in fibroblasts,14 it remains to be determined
which subunits participate in functional complexes in specific cell
types and/or whether as-yet-unidentified proteins take part in
O2-· formation. If
cardiovascular cells contain a neutrophil-like oxidase,
it is essential to identify the electron transport moiety of the
protein. Although gp91phox may serve this function in
endothelial and adventitial cells, its apparent absence
in SMCs suggests that a substitute must exist. Recently, several
homologues of gp91phox have been cloned, and one of them, termed mox-1,
for mitogenic oxidase (now known as nox-1, for
NADPH oxidase), has been shown to be expressed in
VSMCs.15 In these cells, nox-1 mediates the
proliferative response to serum, and nox-1 antisense attenuates
O2-· production in
response to platelet-derived growth factor (PDGF).15
Two other nox proteins have also been found: a 138-kDa protein (tox-1)
that is the main, if not the sole, component of the thyroid
oxidase,16 and a 578amino acid protein,
renox, that is expressed mainly in the kidney.17
Expression of these oxidases in vascular cells and their interaction
with other phox subunits remain to be determined.
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Regulation of ROS Production by Vasoactive Agonists and
Mechanical Forces
There is good evidence for agonist-induced ROS production
in both SMCs and endothelial cells. One of the first
reports that the vascular NAD(P)H oxidase was hormone sensitive showed
that Ang II treatment of SMCs increases intracellular
O2-·
production.4 Ang IIstimulated
O2-· is converted to
H2O2 as early as 1 minute
after addition of hormone.18 Superoxide production
in response to Ang II occurs when either NADH or NADPH is used as a
substrate and is inhibitable by diphenylene iodonium (DPI), a compound
that binds to and inhibits flavin-containing oxidases; Tiron, an
O2-· scavenger;
N-acetylcysteine (NAC), which increases intracellular
glutathione pools; and SOD.4 Treatment with antisense
p22phox to depress NAD(P)H oxidase expression also blocks Ang
IIinduced O2-·
production.12 Activation of this oxidase by
Ang II appears to involve arachidonic acid
metabolites,19 perhaps derived ultimately from
phospholipase Dmediated phosphatidylcholine
hydrolysis.20 Ang II also stimulates NAD(P)H-dependent
O2-· production in
endothelial cells21 22 23 and adventitial
fibroblasts.14
Other agonists and mechanical forces have also been shown to increase
ROS production in vascular cells. PDGF, thrombin, TNF-
, and
lactosylceramide activate NAD(P)H oxidasedependent
O2-· production in
SMCs.6 7 24 25 26 Fibroblasts exhibit increased NADH- or
NADPH-driven O2-·
production in response to TNF-
, IL-1, and
platelet-activating factor.27 28 In
endothelial cells, mechanical forces, including cyclic
stretch and laminar and oscillatory shear stress, stimulate NAD(P)H
oxidase activity.29 30 The upstream signals responsible
for oxidase activation in each of these cell types with each of these
stimuli remain to be established.
Signal Transduction Pathways Modulated by ROS
In order for ROS to modify the response of a cell to an agonist,
it must affect specific signaling cascades. Over the past several
years, many redox-sensitive proteins have been identified, and in some
cases, it has been shown that hormonal activation is mediated by ROS.
Often, both redox-sensitive and redox-insensitive pathways contribute
to activation of a particular enzyme (Figure 2
). The relationship between signaling
cascades known to respond to ROS is depicted in Figure 2
, and each pathway is discussed individually below.
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Proximal Tyrosine Kinases
Growing evidence indicates that the epidermal growth factor
receptor (EGF-R) and the PDGF receptor (PDGF-R) serve not only as
receptors for EGF and PDGF, respectively, but also as a scaffold for
assembly of signaling complexes by G proteincoupled receptors such as
those for Ang II.31 32 It is of interest that
transactivation of both of these growth factor receptors is redox
sensitive. In SMCs, H2O2
induces tyrosine phosphorylation of the EGF-R and
stimulates its association with Shc (src homology complex)Grb2
(growth factor receptorbound protein 2)Sos (son-of-sevenless)
complex to activate subsequent signaling cascades (Figure 2
).33 Furthermore, Ang IIinduced EGF-R
transactivation is mediated through NAD(P)H oxidasederived ROS
because it is strongly inhibited by several antioxidants in SMCs and by
NAC in cardiac fibroblasts.34 35 Heeneman et
al36 have most recently reported that Ang IIinduced
phosphorylation of the Shc/PDGFß-R complex is
mediated by ROS.
Although phosphorylation of the EGF-R by Ang II
is redox sensitive, phosphorylation by EGF is not,
suggesting that an even more proximal kinase than the EGF-R exists.
Recently, we have shown that this kinase is c-Src.34 c-Src
is an important signaling molecule with many functions: it
phosphorylates phospholipase C-
37 ; forms
complexes with the EGF-R,32 paxillin,38
and Janus kinase (JAK)-239 ; and mediates activation
of mitogen-activated protein kinases (MAPKs).40 In
mouse fibroblasts, H2O2
directly activates c-Src.40 Moreover, Ang
IIinduced c-Src phosphorylation at both the
autophosphorylation site (Y418) and the
SH2-domain (Y215) is inhibited by antioxidants,
suggesting that in VSMCs,
H2O2 is a proximal mediator
of agonist-induced c-Src activation.34
Another signaling molecule that is activated quite early after
receptor stimulation is the low-molecular-weight GTP-binding protein
Ras. Ras has a dual role in redox-sensitive signaling: it mediates
activation of the NADH/NADPH oxidase to generate intracellular
ROS,5 and it is also activated by ROS in vivo and
in vitro.41 42 43 ROS activate Ras via an oxidative
modification of cysteine-118, leading to inhibition of the GDP-GTP
exchange.42 Moreover, ROS-triggered Ras activation induces
recruitment of phosphatidylinositol 3'-kinase to Ras, an event that is
required for activation of downstream signals such as Akt and MAPK
(Figure 2
and below).44
Mitogen-Activated Protein Kinases
The MAPKs are a family of serine/threonine kinases that control
cellular responses to growth, apoptosis, and stress signals.
There are 4 main MAPKs, including extracellular signalregulated
kinases (ERK1/2), c-Jun N-terminal kinases (JNKs, also
termed SAPKs), p38 MAPKs, and big MAPK-1. These proteins are the best
studied in terms of their redox sensitivity. In SMCs,
H2O2 has been shown to
activate p38 MAPK,45 46 JNK,46
and big MAPK-1.47 Its effects on ERK1/2 are controversial,
with some reports showing inhibition and others demonstrating
stimulation.45 46 48 49 In terms of agonist-induced
activation of these enzymes, it has been clearly demonstrated that p38
MAPK and JNK activation by Ang II is inhibited by antioxidants (DPI,
NAC), p22phox antisense, or overexpression of
catalase.45 50 Recently, it has been shown that
arachidonic acid stimulates JNK via Rac-1dependent
H2O2
production.51 Because arachidonic
acid is produced in response to many vasoactive hormones, this may
represent a common mechanism of activation. Moreover, although
PDGF-induced ERK1/2 phosphorylation is inhibited by
incubation with catalase,25 Ang II activation of these
enzymes is not.45 49 50
In endothelial cells, H2O2 activates p38 MAPK and its downstream target, MAPK-activated protein (MAPKAP) kinase 2/3, leading to phosphorylation of heat-shock protein 27 (Hsp27).52 53 ERK1/2 activation also seems to be redox sensitive in this cell type, based on the observation that shear stressinduced ERK1/2 phosphorylation is inhibited by antioxidants and dominant-negative Rac-1.54 In neonatal rat ventricular myocytes, all 3 MAPKs (ERK1/2, p38 MAPK, and JNK) have been demonstrated to be activated by H2O2.55 Thus, regulation of MAPK activity by ROS varies not only among family members but also among cells.
Akt
The recently identified serine/threonine kinase Akt/protein kinase
B has been shown to play a key role in many cellular processes,
including cell survival and protein synthesis.56 Akt
inhibits glycogen synthase kinase 3 and activates p70S6K and
the transcription factors activator protein (AP)-1 and
E2F.56 Similar to p38 MAPK, both exogenous
H2O2 and Ang II
activate Akt in SMCs.57 Ang IIinduced Akt
phosphorylation is inhibited by DPI or overexpression
of catalase, suggesting a role for NAD(P)H oxidasederived ROS in
agonist-induced Akt activation.
H2O2 stimulation of Akt has
also been reported in other nonvascular cell types, including NIH3T3
fibroblasts, human embryonic kidney 293 cells, and HeLa and Jurkat
cells.58 59 60 It is noteworthy that Konishi et
al59 demonstrated that
H2O2-induced Akt activation
caused association with Hsp27, which itself is also
phosphorylated by
H2O2.52 61
Furthermore, MAPKAP kinase-2, a substrate of p38
MAPK,62 63 can phosphorylate Akt in
vitro,64 65 raising the possibility that
H2O2 may
phosphorylate both Akt and Hsp27 by activation of p38
MAPK.
Other Candidate Redox-Sensitive Enzymes
Most likely, we have only scratched the surface of the cadre of
oxidant-sensitive signaling pathways. Many proteins, including
phospholipase D, Fyn, proline-rich tyrosine kinase (Pyk) 2, JAK2, and
signal transducer and activator of transcription (STAT) 1,
appear to be redox sensitive, based on their activation by addition of
exogenous ROS. For example,
H2O2 and lipid
hydroperoxides activate phospholipase D in
endothelial cells.66 In mouse fibroblasts,
H2O2 activates JAK2
via Fyn kinase, resulting in the stimulation of Ras
activity.67 Pyk2 has also been reported to be redox
sensitive, because H2O2 and
the strong oxidant diamide both increase Pyk2
phosphorylation.68 Furthermore,
PDGF-induced STAT activation is inhibited by antioxidants such as NAC
and DPI.69 Although, for the most part, the role of ROS in
activation of these pathways by agonists has not been studied, their
clear relationship with ROS suggests that they are potentially among
the proteins that mediate redox-sensitive
physiological responses.
| Regulation of Gene Expression by ROS |
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and lactosylceramide
induction of intercellular adhesion molecule (ICAM-1)26 71
and Ang II, PDGF, and TNF-
stimulation of monocyte chemotactic
protein (MCP)-1.24 72 In contrast, stimulation of MCP-1 by
IL-1ß24 in VSMCs is not affected by antioxidants,
suggesting that the control of gene expression by ROS is both stimulus
and tissue specific.
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Induction of several genes by cytokines is inhibited by NO donors, including vascular cell adhesion molecule (VCAM)-1,73 74 ICAM-1,73 and monocyte colony-stimulating factor (M-CSF).75 This is an interesting mechanism of regulation because NO· appears to act in a cGMP-independent manner to inhibit expression at the level of transcription.76 Not only can NO· alter the activity and expression of transcription factors, but also it scavenges O2-· to form peroxynitrite, thus modulating O2-·-dependent transcription as well.
Regulation of gene expression by oxidant stress occurs at various
levels. In some cases, regulation of the gene is redox sensitive owing
to the susceptibility of upstream signaling pathways to ROS. For
example, induction of early growth response (Egr)-1 by cyclic strain
has been shown to depend on redox-sensitive activation of the
Ras-Raf-ERK1/2 pathway.77 Moreover,
H2O2-induced AP-1 binding
in porcine aortic endothelial cells requires activation
of Src.78 In other cases, ROS mediate increased turnover,
expression, or translocation of specific transcription factors, thus
modifying their activity. This mechanism has been shown to be effective
for both the nuclear factor (NF)-
B and AP-1 transcription factors.
Hydroperoxy fatty acids and
H2O2 increase the
expression of Fos and Jun, 2 proteins that form heterodimers and
activate AP-1.79 NO· increases the transcription
of I
B, the inhibitory factor that binds NF-
B and
causes retention of this transcription factor in a cytoplasmic,
inactive form.73 The turnover of I
B protein is also
oxidant sensitive: antioxidants can prevent agonist-stimulated I
B
phosphorylation and degradation.73
Conversely, H2O2 increases
nuclear translocation of NF-
B, contributing to the induction of
genes responsive to this transcription factor.78
An additional level of redox regulation of gene expression is that the
affinity of certain transcription factors for their cognate DNA-binding
sites can be directly modified by ROS. This mechanism was first
identified in bacteria, where excess
H2O2 interacts with the
oxyR regulon, and O2-· or
NO· activates the SoxRS regulon to control the expression of
a subset of genes, including MnSOD and aconitase.80 The
oxyR-binding motif has also been shown to function as a redox-sensitive
transcriptional enhancer in mammalian cells.81 Since then,
several mammalian transcription factors have been shown to be directly
modified by ROS or by reducing proteins that modify cysteine residues
involved in DNA binding. Transcription factors in this category include
AP-1, NF-
B, and most likely hypoxia-inducible factor
(HIF)-1.82 83 Both Fos and Jun have a conserved cysteine
in a basic motif that, when oxidized, interferes with the binding of
these proteins to AP-1 consensus sequences. Conversely, if Fos/Jun
heterodimers are bound to AP-1, they cannot be oxidized.82
The oxidation state of these important proteins is controlled by redox
factor (REF)-1, a protein that, in cooperation with thioredoxin,
promotes the cycling of the critical cysteines between reduced and
oxidized forms.82 84 Thioredoxin also regulates
HIF-1dependent transcription83 and modifies the DNA
binding and transcriptional activity of NF-
B by reducing cysteine
62.85 These studies clearly indicate the importance of the
nuclear redox state in regulating gene expression.
| Role of ROS in Vascular Physiology and Pathophysiology |
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Vascular Smooth Muscle Growth, Hypertrophy, and
Apoptosis
A characteristic of hypertension is hypertrophy of
large vessels.86 We have demonstrated that Ang IIinduced
hypertrophy of SMCs is dependent on intracellularly
produced H2O2, which is
derived, at least in part, from an NAD(P)H oxidase.4 12 18
Ang IIinduced hypertrophy can be inhibited by
DPI,4 attenuation of NAD(P)H oxidase activity by
transfection of antisense p22phox,12 and catalase
overexpression.18 Similar findings were reported for
cardiac myocytes, in which Ang IIinduced hypertrophy was
associated with intracellular production of ROS and was blocked
by antioxidants.87
Other vascular disorders such as restenosis have a significant proliferative component, resulting from SMC and/or fibroblast migration and multiplication in the neointima.88 Sundaresan et al25 demonstrated a clear requirement for H2O2 in PDGF-induced proliferation. Migration in response to this agonist is also inhibited by catalase, suggesting that it, too, is mediated by ROS. Similar results were found by Brown et al,89 who showed that overexpression of catalase in SMCs not only inhibited serum-induced [3H]thymidine incorporation and proliferation but also promoted apoptosis. Phenylephrine-induced proliferation of rabbit aortic SMCs has also been shown to require H2O2.90 Proof that balloon angioplasty increases oxidant stress has been provided in 2 studies. Within 30 minutes after injury, glutathione levels fall by 63%, coincident with medial smooth muscle apoptosis, suggesting that this early step in the response to injury is associated with severe oxidant stress. Importantly, administration of NAC or pyrrolidine dithiocarbamate prevents the glutathione loss and the smooth muscle apoptosis.91 In another study, Nunes et al92 showed that vascular O2-· was increased 2.5-fold in injured arteries compared with uninjured controls. Moreover, treatment with either probucol or the combination of vitamins C and E normalized O2-· levels and partially suppressed neointimal formation.93 Davies et al94 have recently reported that p38 MAPK is upregulated after injury, suggesting that this signaling pathway might also be a redox-sensitive target in vivo.
Endothelial Dysfunction
Endothelial dysfunction is a hallmark of multiple
vascular diseases, including hypertension,
atherosclerosis, and diabetes mellitus. Impaired
endothelial function has several consequences, the most
important of which is decreased endothelium-dependent
vasodilation. The endothelial cell redox rheostat is
primarily regulated by the dynamic production of and
interaction between NO· and
O2-·. NO· is the most
potent endogenous vasodilator and inhibits smooth muscle
proliferation and migration, adhesion of leukocytes to the
endothelium, and platelet
aggregation.95 In cholesterol-fed rabbits,
O2-· is increased in the
aorta,96 and treatment with polyethylene glycolSOD
reverses the impairment in endothelium-dependent
relaxation.97 In the same animal model, treatment with
probucol (a lipid-lowering agent with potent antioxidant properties)
corrects endothelial dysfunction and lowers
O2-·.98 Impaired
endothelium-dependent vasodilation also occurs in
hypertension, such as that produced by infusion of rats with Ang
II,3 restriction of blood flow to 1 kidney,99
and administration of deoxycorticosterone acetate-salt.100
The endothelial dysfunction that accompanies Ang II
infusion or deoxycorticosterone acetate-salt can be corrected by
administration of liposomal or matrix-targeted
SOD,100 101 102 providing further proof that ROS, and
specifically O2-·, are
involved in this response.
The Inflammatory Response
Another consequence of endothelial dysfunction and
SMC activation is increased monocyte adhesion, foam cell formation, and
thrombosis. As noted above, pro-oxidant agonists such as Ang II and
TNF-
induce the expression of proinflammatory molecules such as
VCAM-1, MCP-1, and the thrombin receptor.6 72 103 104 105 106
Each of these molecules is in turn redox
sensitive,72 104 107 and in the case of MCP-1 and the
thrombin receptor, a role for ROS in Ang IImediated gene expression
has been demonstrated.72 104
Matrix Remodeling
Collagen degradation depends on the activity of enzymes known as
metalloproteinases (MMPs). MMP-2 (gelatinase A, which degrades collagen
IV from the basal membrane) and MMP-9 (gelatinase B, which acts on
collagen I fibers) are secreted by macrophages and vascular
myocytes in an inactive form.108 MMP-9 expression is
increased in the shoulder region of atherosclerotic plaques; ie, in the
sites prone to plaque rupture.109 Rajagopalan et
al110 demonstrated that proMMP-9 and proMMP2 secreted
into the medium of cultured human SMCs are activated by ROS.
Moreover, NAC treatment prevents MMP-9 expression and activation in
hypercholesterolemic rabbits,111
suggesting a mechanism for how antioxidants may contribute to plaque
stabilization.
| Conclusions and Future Directions |
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| Acknowledgments |
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Received May 26, 2000; accepted August 10, 2000.
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T. Matsuno, Y. Ito, T. Ohashi, M. Morise, N. Takeda, K. Shimokata, K. Imaizumi, H. Kume, and Y. Hasegawa Dual Pathway Activated by tert-Butyl Hydroperoxide in Human Airway Anion Secretion J. Pharmacol. Exp. Ther., November 1, 2008; 327(2): 453 - 464. [Abstract] [Full Text] [PDF] |
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D. Liu, L. Gao, S. K. Roy, K. G. Cornish, and I. H. Zucker Role of Oxidant Stress on AT1 Receptor Expression in Neurons of Rabbits With Heart Failure and in Cultured Neurons Circ. Res., July 18, 2008; 103(2): 186 - 193. [Abstract] [Full Text] [PDF] |
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M. J. Haurani, M. E. Cifuentes, A. D. Shepard, and P. J. Pagano Nox4 Oxidase Overexpression Specifically Decreases Endogenous Nox4 mRNA and Inhibits Angiotensin II-Induced Adventitial Myofibroblast Migration Hypertension, July 1, 2008; 52(1): 143 - 149. [Abstract] [Full Text] [PDF] |
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V. Mollace, S. Ragusa, I. Sacco, C. Muscoli, F. Sculco, V. Visalli, E. Palma, S. Muscoli, L. Mondello, P. Dugo, et al. The Protective Effect of Bergamot Oil Extract on Lecitine-like OxyLDL Receptor-1 Expression in Balloon Injury-related Neointima Formation Journal of Cardiovascular Pharmacology and Therapeutics, June 1, 2008; 13(2): 120 - 129. [Abstract] [PDF] |
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N. Sud, S. M. Wells, S. Sharma, D. A. Wiseman, J. Wilham, and S. M. Black Asymmetric dimethylarginine inhibits HSP90 activity in pulmonary arterial endothelial cells: role of mitochondrial dysfunction Am J Physiol Cell Physiol, June 1, 2008; 294(6): C1407 - C1418. [Abstract] [Full Text] [PDF] |
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V. G. DeMarco, J. Habibi, A. T. Whaley-Connell, R. I. Schneider, R. L. Heller, J. P. Bosanquet, M. R. Hayden, K. Delcour, S. A. Cooper, B. T. Andresen, et al. Oxidative stress contributes to pulmonary hypertension in the transgenic (mRen2)27 rat Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2659 - H2668. [Abstract] [Full Text] [PDF] |
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M. Takahashi, E. Suzuki, R. Takeda, S. Oba, H. Nishimatsu, K. Kimura, T. Nagano, R. Nagai, and Y. Hirata Angiotensin II and tumor necrosis factor-{alpha} synergistically promote monocyte chemoattractant protein-1 expression: roles of NF-{kappa}B, p38, and reactive oxygen species Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2879 - H2888. [Abstract] [Full Text] [PDF] |
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K. E. Herbert, Y. Mistry, R. Hastings, T. Poolman, L. Niklason, and B. Williams Angiotensin II-Mediated Oxidative DNA Damage Accelerates Cellular Senescence in Cultured Human Vascular Smooth Muscle Cells via Telomere-Dependent and Independent Pathways Circ. Res., February 1, 2008; 102(2): 201 - 208. [Abstract] [Full Text] [PDF] |
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T. M. Paravicini and R. M. Touyz NADPH Oxidases, Reactive Oxygen Species, and Hypertension: Clinical implications and therapeutic possibilities Diabetes Care, February 1, 2008; 31(Supplement_2): S170 - S180. [Abstract] [Full Text] [PDF] |
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H. Choi, T. L. Leto, L. Hunyady, K. J. Catt, Y. S. Bae, and S. G. Rhee Mechanism of Angiotensin II-induced Superoxide Production in Cells Reconstituted with Angiotensin Type 1 Receptor and the Components of NADPH Oxidase J. Biol. Chem., January 4, 2008; 283(1): 255 - 267. [Abstract] [Full Text] [PDF] |
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V. W.T. Liu and P. L. Huang Cardiovascular roles of nitric oxide: A review of insights from nitric oxide synthase gene disrupted mice Cardiovasc Res, January 1, 2008; 77(1): 19 - 29. [Abstract] [Full Text] [PDF] |
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J. D. Erusalimsky and S. Moncada Nitric Oxide and Mitochondrial Signaling: From Physiology to Pathophysiology Arterioscler Thromb Vasc Biol, December 1, 2007; 27(12): 2524 - 2531. [Abstract] [Full Text] [PDF] |
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L.-J. Min, M. Mogi, J. Iwanami, J.-M. Li, A. Sakata, T. Fujita, K. Tsukuda, M. Iwai, and M. Horiuchi Cross-talk between aldosterone and angiotensin II in vascular smooth muscle cell senescence Cardiovasc Res, December 1, 2007; 76(3): 506 - 516. [Abstract] [Full Text] [PDF] |
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T. Adachi, M. Yamamoto, and M. Suematsu Targeting NAD(P)H Oxidase: Ets-1 Regulates p47phox Circ. Res., November 9, 2007; 101(10): 962 - 964. [Full Text] [PDF] |
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W. Ni, Y. Zhan, H. He, E. Maynard, J. A. Balschi, and P. Oettgen Ets-1 Is a Critical Transcriptional Regulator of Reactive Oxygen Species and p47phox Gene Expression in Response to Angiotensin II Circ. Res., November 9, 2007; 101(10): 985 - 994. [Abstract] [Full Text] [PDF] |
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M. J. Haurani and P. J. Pagano Adventitial fibroblast reactive oxygen species as autacrine and paracrine mediators of remodeling: Bellwether for vascular disease? Cardiovasc Res, September 1, 2007; 75(4): 679 - 689. [Abstract] [Full Text] [PDF] |
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J. P. Luyendyk, J. D. Piper, M. Tencati, K. V. Reddy, T. Holscher, R. Zhang, J. Luchoomun, X. Chen, W. Min, C. Kunsch, et al. A Novel Class of Antioxidants Inhibit LPS Induction of Tissue Factor by Selective Inhibition of the Activation of ASK1 and MAP Kinases Arterioscler Thromb Vasc Biol, August 1, 2007; 27(8): 1857 - 1863. [Abstract] [Full Text] [PDF] |
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A. Pirillo, P. Uboldi, G. Pappalardo, H. Kuhn, and A. L. Catapano Modification of HDL3 by mild oxidative stress increases ATP-binding cassette transporter 1-mediated cholesterol efflux Cardiovasc Res, August 1, 2007; 75(3): 566 - 574. [Abstract] [Full Text] [PDF] |
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J. Kitayama, F. M. Faraci, S. R. Lentz, and D. D. Heistad Cerebral Vascular Dysfunction During Hypercholesterolemia Stroke, July 1, 2007; 38(7): 2136 - 2141. [Abstract] [Full Text] [PDF] |
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S. S. Barbieri and B. B. Weksler Tobacco smoke cooperates with interleukin-1{beta} to alter {beta}-catenin trafficking in vascular endothelium resulting in increased permeability and induction of cyclooxygenase-2 expression in vitro and in vivo FASEB J, June 1, 2007; 21(8): 1831 - 1843. [Abstract] [Full Text] [PDF] |
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L. Ding, A. Chapman, R. Boyd, and H. D. Wang ERK activation contributes to regulation of spontaneous contractile tone via superoxide anion in isolated rat aorta of angiotensin II-induced hypertension Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2997 - H3005. [Abstract] [Full Text] [PDF] |
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M. Yusof, K. Kamada, F. Spencer Gaskin, and R. J. Korthuis Angiotensin II mediates postischemic leukocyte-endothelial interactions: role of calcitonin gene-related peptide Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H3032 - H3037. [Abstract] [Full Text] [PDF] |
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P. Larghero, R. Vene, S. Minghelli, G. Travaini, M. Morini, N. Ferrari, U. Pfeffer, D. M. Noonan, A. Albini, and R. Benelli Biological assays and genomic analysis reveal lipoic acid modulation of endothelial cell behavior and gene expression Carcinogenesis, May 1, 2007; 28(5): 1008 - 1020. [Abstract] [Full Text] [PDF] |
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D. N. Mayorov Brain superoxide as a key regulator of the cardiovascular response to emotional stress in rabbits Exp Physiol, May 1, 2007; 92(3): 471 - 479. [Abstract] [Full Text] [PDF] |
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A. Alcaraz, D. Iyu, N. M. Atucha, J. Garcia-Estan, and M. C. Ortiz Vitamin E supplementation reverses renal altered vascular reactivity in chronic bile duct-ligated rats Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2007; 292(4): R1486 - R1493. [Abstract] [Full Text] [PDF] |
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J. Liu, T. Shimosawa, H. Matsui, F. Meng, S. C. Supowit, D. J. DiPette, K. Ando, and T. Fujita Adrenomedullin inhibits angiotensin II-induced oxidative stress via Csk-mediated inhibition of Src activity Am J Physiol Heart Circ Physiol, April 1, 2007; 292(4): H1714 - H1721. [Abstract] [Full Text] [PDF] |
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A. Chakraborty, H. Brooks, P. Zhang, W. Smith, M. R. McReynolds, J. B. Hoying, R. Bick, L. Truong, B. Poindexter, H. Lan, et al. Stanniocalcin-1 regulates endothelial gene expression and modulates transendothelial migration of leukocytes Am J Physiol Renal Physiol, February 1, 2007; 292(2): F895 - F904. [Abstract] [Full Text] [PDF] |
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K. Bedard and K.-H. Krause The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology Physiol Rev, January 1, 2007; 87(1): 245 - 313. [Abstract] [Full Text] [PDF] |
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K. Thakali, L. Davenport, G. D. Fink, and S. W. Watts Cyclooxygenase, p38 Mitogen-Activated Protein Kinase (MAPK), Extracellular Signal-Regulated Kinase MAPK, Rho Kinase, and Src Mediate Hydrogen Peroxide-Induced Contraction of Rat Thoracic Aorta and Vena Cava J. Pharmacol. Exp. Ther., January 1, 2007; 320(1): 236 - 243. [Abstract] [Full Text] [PDF] |
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Z. Orosz, A. Csiszar, N. Labinskyy, K. Smith, P. M. Kaminski, P. Ferdinandy, M. S. Wolin, A. Rivera, and Z. Ungvari Cigarette smoke-induced proinflammatory alterations in the endothelial phenotype: role of NAD(P)H oxidase activation Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H130 - H139. [Abstract] [Full Text] [PDF] |
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F.-Y. Lin, Y.-H. Chen, Y.-W. Lin, J.-S. Tsai, J.-W. Chen, H.-J. Wang, Y.-L. Chen, C.-Y. Li, and S.-J. Lin The Role of Human Antigen R, an RNA-binding Protein, in Mediating the Stabilization of Toll-Like Receptor 4 mRNA Induced by Endotoxin: A Novel Mechanism Involved in Vascular Inflammation Arterioscler Thromb Vasc Biol, December 1, 2006; 26(12): 2622 - 2629. [Abstract] [Full Text] [PDF] |
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F.-Y. Lin, Y.-H. Chen, J.-S. Tasi, J.-W. Chen, T.-L. Yang, H.-J. Wang, C.-Y. Li, Y.-L. Chen, and S.-J. Lin Endotoxin Induces Toll-Like Receptor 4 Expression in Vascular Smooth Muscle Cells via NADPH Oxidase Activation and Mitogen-Activated Protein Kinase Signaling Pathways Arterioscler Thromb Vasc Biol, December 1, 2006; 26(12): 2630 - 2637. [Abstract] [Full Text] [PDF] |
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M. Ushio-Fukai and R. W. Alexander Caveolin-Dependent Angiotensin II Type 1 Receptor Signaling in Vascular Smooth Muscle Hypertension, November 1, 2006; 48(5): 797 - 803. [Full Text] [PDF] |
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C. E. Murdoch, M. Zhang, A. C. Cave, and A. M. Shah NADPH oxidase-dependent redox signalling in cardiac hypertrophy, remodelling and failure Cardiovasc Res, July 15, 2006; 71(2): 208 - 215. [Abstract] [Full Text] [PDF] |
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R. E. Clempus and K. K. Griendling Reactive oxygen species signaling in vascular smooth muscle cells Cardiovasc Res, July 15, 2006; 71(2): 216 - 225. [Abstract] [Full Text] [PDF] |
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T. M. Paravicini and R. M. Touyz Redox signaling in hypertension Cardiovasc Res, July 15, 2006; 71(2): 247 - 258. [Abstract] [Full Text] [PDF] |
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K. V. Ramana, A. Bhatnagar, S. Srivastava, U. C. Yadav, S. Awasthi, Y. C. Awasthi, and S. K. Srivastava Mitogenic Responses of Vascular Smooth Muscle Cells to Lipid Peroxidation-derived Aldehyde 4-Hydroxy-trans-2-nonenal (HNE): ROLE OF ALDOSE REDUCTASE-CATALYZED REDUCTION OF THE HNE-GLUTATHIONE CONJUGATES IN REGULATING CELL GROWTH J. Biol. Chem., June 30, 2006; 281(26): 17652 - 17660. [Abstract] [Full Text] [PDF] |
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P. J. Pagano and M. J. Haurani Vascular Cell Locomotion: Osteopontin, NADPH Oxidase, and Matrix Metalloproteinase-9 Circ. Res., June 23, 2006; 98(12): 1453 - 1455. [Full Text] [PDF] |
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M. Weaver, J. Liu, D. Pimentel, D. J. Reddy, P. Harding, E. L. Peterson, and P. J. Pagano Adventitial delivery of dominant-negative p67phox attenuates neointimal hyperplasia of the rat carotid artery Am J Physiol Heart Circ Physiol, May 1, 2006; 290(5): H1933 - H1941. [Abstract] [Full Text] [PDF] |
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N. Ardanaz and P. J. Pagano Hydrogen peroxide as a paracrine vascular mediator: regulation and signaling leading to dysfunction. Experimental Biology and Medicine, March 1, 2006; 231(3): 237 - 251. [Abstract] [Full Text] [PDF] |
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J. A. Polikandriotis, H. L. Rupnow, S. C. Elms, R. E. Clempus, D. J. Campbell, R. L. Sutliff, L. A. S. Brown, D. M. Guidot, and C. M. Hart Chronic Ethanol Ingestion Increases Superoxide Production and NADPH Oxidase Expression in the Lung Am. J. Respir. Cell Mol. Biol., March 1, 2006; 34(3): 314 - 319. [Abstract] [Full Text] [PDF] |
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A. Cave, D. Grieve, S. Johar, M. Zhang, and A. M Shah NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology Phil Trans R Soc B, December 29, 2005; 360(1464): 2327 - 2334. [Abstract] [Full Text] [PDF] |
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L. Cheng, W. Cao, C. Fiocchi, J. Behar, P. Biancani, and K. M. Harnett In vitro model of acute esophagitis in the cat Am J Physiol Gastrointest Liver Physiol, November 1, 2005; 289(5): G860 - G869. [Abstract] [Full Text] [PDF] |
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N. Li, G. Zhang, F.-X. Yi, A.-P. Zou, and P.-L. Li Activation of NAD(P)H oxidase by outward movements of H+ ions in renal medullary thick ascending limb of Henle Am J Physiol Renal Physiol, November 1, 2005; 289(5): F1048 - F1056. [Abstract] [Full Text] [PDF] |
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T. Suvorava, N. Lauer, S. Kumpf, R. Jacob, W. Meyer, and G. Kojda Endogenous Vascular Hydrogen Peroxide Regulates Arteriolar Tension In Vivo Circulation, October 18, 2005; 112(16): 2487 - 2495. [Abstract] [Full Text] [PDF] |
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S. H.H. Chan, K.-S. Hsu, C.-C. Huang, L.-L. Wang, C.-C. Ou, and J. Y.H. Chan NADPH Oxidase-Derived Superoxide Anion Mediates Angiotensin II-Induced Pressor Effect via Activation of p38 Mitogen-Activated Protein Kinase in the Rostral Ventrolateral Medulla Circ. Res., October 14, 2005; 97(8): 772 - 780. [Abstract] [Full Text] [PDF] |
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C. De Ciuceis, F. Amiri, P. Brassard, D. H. Endemann, R. M. Touyz, and E. L. Schiffrin Reduced Vascular Remodeling, Endothelial Dysfunction, and Oxidative Stress in Resistance Arteries of Angiotensin II-Infused Macrophage Colony-Stimulating Factor-Deficient Mice: Evidence for a Role in Inflammation in Angiotensin-Induced Vascular Injury Arterioscler Thromb Vasc Biol, October 1, 2005; 25(10): 2106 - 2113. [Abstract] [Full Text] [PDF] |
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L. Zuo, M. Ushio-Fukai, S. Ikeda, L. Hilenski, N. Patrushev, and R. W. Alexander Caveolin-1 Is Essential for Activation of Rac1 and NAD(P)H Oxidase After Angiotensin II Type 1 Receptor Stimulation in Vascular Smooth Muscle Cells: Role in Redox Signaling and Vascular Hypertrophy Arterioscler Thromb Vasc Biol, September 1, 2005; 25(9): 1824 - 1830. [Abstract] [Full Text] [PDF] |
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D. K. Jagadeesha, T. E. Lindley, J. DeLeon, R. V. Sharma, F. Miller, and R. C. Bhalla Tempol therapy attenuates medial smooth muscle cell apoptosis and neointima formation after balloon catheter injury in carotid artery of diabetic rats Am J Physiol Heart Circ Physiol, September 1, 2005; 289(3): H1047 - H1053. [Abstract] [Full Text] [PDF] |
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T. Berg Increased counteracting effect of eNOS and nNOS on an {alpha}1-adrenergic rise in total peripheral vascular resistance in spontaneous hypertensive rats Cardiovasc Res, September 1, 2005; 67(4): 736 - 744. [Abstract] [Full Text] [PDF] |
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J. W. Zmijewski, D. R. Moellering, C. L. Goffe, A. Landar, A. Ramachandran, and V. M. Darley-Usmar Oxidized LDL induces mitochondrially associated reactive oxygen/nitrogen species formation in endothelial cells Am J Physiol Heart Circ Physiol, August 1, 2005; 289(2): H852 - H861. [Abstract] [Full Text] [PDF] |
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P. L. Huang Unraveling the Links Between Diabetes, Obesity, and Cardiovascular Disease Circ. Res., June 10, 2005; 96(11): 1129 - 1131. [Full Text] [PDF] |
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G. Desideri, M. De Simone, L. Iughetti, T. Rosato, M. L. Iezzi, M. C. Marinucci, V. Cofini, G. Croce, G. Passacquale, S. Necozione, et al. Early Activation of Vascular Endothelial Cells and Platelets in Obese Children J. Clin. Endocrinol. Metab., June 1, 2005; 90(6): 3145 - 3152. [Abstract] [Full Text] [PDF] |
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M. Akishita, K. Nagai, H. Xi, W. Yu, N. Sudoh, T. Watanabe, M. Ohara-Imaizumi, S. Nagamatsu, K. Kozaki, M. Horiuchi, et al. Renin-Angiotensin System Modulates Oxidative Stress-Induced Endothelial Cell Apoptosis in Rats Hypertension, June 1, 2005; 45(6): 1188 - 1193. [Abstract] [Full Text] [PDF] |
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F. Krotz, B. Engelbrecht, M. A. Buerkle, F. Bassermann, H. Bridell, T. Gloe, J. Duyster, U. Pohl, and H.-Y. Sohn The Tyrosine Phosphatase, SHP-1, Is a Negative Regulator of Endothelial Superoxide Formation J. Am. Coll. Cardiol., May 17, 2005; 45(10): 1700 - 1706. [Abstract] [Full Text] [PDF] |
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T. M. Griffith, A. T. Chaytor, L. M. Bakker, and D. H. Edwards 5-Methyltetrahydrofolate and tetrahydrobiopterin can modulate electrotonically mediated endothelium-dependent vascular relaxation PNAS, May 10, 2005; 102(19): 7008 - 7013. [Abstract] [Full Text] [PDF] |
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J. I. Mendez, W. J. Nicholson, and W. R. Taylor SOD Isoforms and Signaling in Blood Vessels: Evidence for the Importance of ROS Compartmentalization Arterioscler Thromb Vasc Biol, May 1, 2005; 25(5): 887 - 888. [Full Text] [PDF] |
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C. Kunsch, J. Luchoomun, X.-l. Chen, G. L. Dodd, K. S. Karu, C. Q. Meng, E. M. Marino, L. K. Olliff, J. D. Piper, F.-H. Qiu, et al. J. Pharmacol. Exp. Ther., May 1, 2005; 313(2): 492 - 501. [Abstract] [Full Text] [PDF] |
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P.-C. Lee, I-C. Ho, and T.-C. Lee Oxidative Stress Mediates Sodium Arsenite-Induced Expression of Heme Oxygenase-1, Monocyte Chemoattractant Protein-1, and Interleukin-6 in Vascular Smooth Muscle Cells Toxicol. Sci., May 1, 2005; 85(1): 541 - 550. [Abstract] [Full Text] [PDF] |
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T. Ago, T. Kitazono, J. Kuroda, Y. Kumai, M. Kamouchi, H. Ooboshi, M. Wakisaka, T. Kawahara, K. Rokutan, S. Ibayashi, et al. NAD(P)H Oxidases in Rat Basilar Arterial Endothelial Cells Stroke, May 1, 2005; 36(5): 1040 - 1046. [Abstract] [Full Text] [PDF] |
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H. Cai NAD(P)H Oxidase-Dependent Self-Propagation of Hydrogen Peroxide and Vascular Disease Circ. Res., April 29, 2005; 96(8): 818 - 822. [Abstract] [Full Text] [PDF] |
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M. Rahmani, J. T. Read, J. M. Carthy, P. C. McDonald, B. W. Wong, M. Esfandiarei, X. Si, Z. Luo, H. Luo, P. S. Rennie, et al. Regulation of the Versican Promoter by the {beta}-Catenin-T-cell Factor Complex in Vascular Smooth Muscle Cells J. Biol. Chem., April 1, 2005; 280(13): 13019 - 13028. [Abstract] [Full Text] [PDF] |
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M. Tsuda, M. Iwai, J.-M. Li, H.-S. Li, L.-J. Min, A. Ide, M. Okumura, J. Suzuki, M. Mogi, H. Suzuki, et al. Inhibitory Effects of AT1 Receptor Blocker, Olmesartan, and Estrogen on Atherosclerosis Via Anti-Oxidative Stress Hypertension, April 1, 2005; 45(4): 545 - 551. [Abstract] [Full Text] [PDF] |
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R. M. Touyz, C. Mercure, Y. He, D. Javeshghani, G. Yao, G. E. Callera, A. Yogi, N. Lochard, and T. L. Reudelhuber Angiotensin II-Dependent Chronic Hypertension and Cardiac Hypertrophy Are Unaffected by gp91phox-Containing NADPH Oxidase Hypertension, April 1, 2005; 45(4): 530 - 537. [Abstract] [Full Text] [PDF] |
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T. Djordjevic, R. S. BelAiba, S. Bonello, J. Pfeilschifter, J. Hess, and A. Gorlach Human Urotensin II Is a Novel Activator of NADPH Oxidase in Human Pulmonary Artery Smooth Muscle Cells Arterioscler Thromb Vasc Biol, March 1, 2005; 25(3): 519 - 525. [Abstract] [Full Text] [PDF] |
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R. E. Haskew-Layton, A. A. Mongin, and H. K. Kimelberg Hydrogen Peroxide Potentiates Volume-sensitive Excitatory Amino Acid Release via a Mechanism Involving Ca2+/Calmodulin-dependent Protein Kinase II J. Biol. Chem., February 4, 2005; 280(5): 3548 - 3554. [Abstract] [Full Text] [PDF] |
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M. Houston, M. A. Julien, S. Parthasarathy, and E. L. Chaikof Oxidized linoleic acid regulates expression and shedding of syndecan-4 Am J Physiol Cell Physiol, February 1, 2005; 288(2): C458 - C466. [Abstract] [Full Text] [PDF] |
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H. M. Dourron, G. M. Jacobson, J. L. Park, J. Liu, D. J. Reddy, M. L. Scheel, and P. J. Pagano Perivascular gene transfer of NADPH oxidase inhibitor suppresses angioplasty-induced neointimal proliferation of rat carotid artery Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H946 - H953. [Abstract] [Full Text] [PDF] |
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D. Lau, H. Mollnau, J. P. Eiserich, B. A. Freeman, A. Daiber, U. M. Gehling, J. Brummer, V. Rudolph, T. Munzel, T. Heitzer, et al. Myeloperoxidase mediates neutrophil activation by association with CD11b/CD18 integrins PNAS, January 11, 2005; 102(2): 431 - 436. [Abstract] [Full Text] [PDF] |
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J. Hongpaisan, C. A. Winters, and S. B. Andrews Strong Calcium Entry Activates Mitochondrial Superoxide Generation, Upregulating Kinase Signaling in Hippocampal Neurons J. Neurosci., December 1, 2004; 24(48): 10878 - 10887. [Abstract] [Full Text] [PDF] |
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I. N. Bratz and N. L. Kanagy Nitric oxide synthase-inhibition hypertension is associated with altered endothelial cyclooxygenase function Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2394 - H2401. [Abstract] [Full Text] [PDF] |
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J.-W. Chen, F.-Y. Lin, Y.-H. Chen, T.-C. Wu, Y.-L. Chen, and S.-J. Lin Carvedilol Inhibits Tumor Necrosis Factor-{alpha}-Induced Endothelial Transcription Factor Activation, Adhesion Molecule Expression, and Adhesiveness to Human Mononuclear Cells Arterioscler Thromb Vasc Biol, November 1, 2004; 24(11): 2075 - 2081. [Abstract] [Full Text] [PDF] |
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C. Muscoli, I. Sacco, W. Alecce, E. Palma, R. Nistico, N. Costa, F. Clementi, D. Rotiroti, F. Romeo, D. Salvemini, et al. The Protective Effect of Superoxide Dismutase Mimetic M40401 on Balloon Injury-Related Neointima Formation: Role of the Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 J. Pharmacol. Exp. Ther., October 1, 2004; 311(1): 44 - 50. [Abstract] [Full Text] [PDF] |
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R. Stocker and J. F. Keaney Jr. Role of Oxidative Modifications in Atherosclerosis Physiol Rev, October 1, 2004; 84(4): 1381 - 1478. [Abstract] [Full Text] [PDF] |
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J. Liu, A. Ormsby, N. Oja-Tebbe, and P. J. Pagano Gene Transfer of NAD(P)H Oxidase Inhibitor to the Vascular Adventitia Attenuates Medial Smooth Muscle Hypertrophy Circ. Res., September 17, 2004; 95(6): 587 - 594. [Abstract] [Full Text] [PDF] |
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R. Vittal, Z. E. Selvanayagam, Y. Sun, J. Hong, F. Liu, K.-V. Chin, and C. S. Yang Gene expression changes induced by green tea polyphenol (-)-epigallocatechin-3-gallate in human bronchial epithelial 21BES cells analyzed by DNA microarray Mol. Cancer Ther., September 1, 2004; 3(9): 1091 - 1099. [Abstract] [Full Text] [PDF] |
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F. M. Faraci and S. P. Didion Vascular Protection: Superoxide Dismutase Isoforms in the Vessel Wall Arterioscler Thromb Vasc Biol, August 1, 2004; 24(8): 1367 - 1373. [Abstract] [Full Text] [PDF] |
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W. Cai, J. C. He, L. Zhu, M. Peppa, C. Lu, J. Uribarri, and H. Vlassara High Levels of Dietary Advanced Glycation End Products Transform Low-Density Lipoprotein Into a Potent Redox-Sensitive Mitogen-Activated Protein Kinase Stimulant in Diabetic Patients Circulation, July 20, 2004; 110(3): 285 - 291. [Abstract] [Full Text] [PDF] |
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T. Adachi, D. R. Pimentel, T. Heibeck, X. Hou, Y. J. Lee, B. Jiang, Y. Ido, and R. A. Cohen S-Glutathiolation of Ras Mediates Redox-sensitive Signaling by Angiotensin II in Vascular Smooth Muscle Cells J. Biol. Chem., July 9, 2004; 279(28): 29857 - 29862. [Abstract] [Full Text] [PDF] |
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C. M. Stolen, G. G. Yegutkin, R. Kurkijarvi, P. Bono, K. Alitalo, and S. Jalkanen Origins of Serum Semicarbazide-Sensitive Amine Oxidase Circ. Res., July 9, 2004; 95(1): 50 - 57. [Abstract] [Full Text] [PDF] |
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M. Young and J. W. Funder Eplerenone, But Not Steroid Withdrawal, Reverses Cardiac Fibrosis in Deoxycorticosterone/ Salt-Treated Rats Endocrinology, July 1, 2004; 145(7): 3153 - 3157. [Abstract] [Full Text] [PDF] |
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T. Yoshimoto, N. Fukai, R. Sato, T. Sugiyama, N. Ozawa, M. Shichiri, and Y. Hirata Antioxidant Effect of Adrenomedullin on Angiotensin II-Induced Reactive Oxygen Species Generation in Vascular Smooth Muscle Cells Endocrinology, July 1, 2004; 145(7): 3331 - 3337. [Abstract] [Full Text] [PDF] |
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I. Kusaka, G. Kusaka, C. Zhou, M. Ishikawa, A. Nanda, D. N. Granger, J. H. Zhang, and J. Tang Role of AT1 receptors and NAD(P)H oxidase in diabetes-aggravated ischemic brain injury Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2442 - H2451. [Abstract] [Full Text] [PDF] |
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B. Jiang, S. Xu, X. Hou, D. R. Pimentel, and R. A. Cohen Angiotensin II Differentially Regulates Interleukin-1-{beta}-inducible NO Synthase (iNOS) and Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression: ROLE OF p38 MAPK J. Biol. Chem., May 7, 2004; 279(19): 20363 - 20368. [Abstract] [Full Text] [PDF] |
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K K Griendling Novel NAD(P)H oxidases in the cardiovascular system Heart, May 1, 2004; 90(5): 491 - 493. [Full Text] [PDF] |
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G. Ceolotto, M. Bevilacqua, I. Papparella, E. Baritono, L. Franco, C. Corvaja, M. Mazzoni, A. Semplicini, and A. Avogaro Insulin Generates Free Radicals by an NAD(P)H, Phosphatidylinositol 3'-Kinase-Dependent Mechanism in Human Skin Fibroblasts Ex Vivo Diabetes, May 1, 2004; 53(5): 1344 - 1351. [Abstract] [Full Text] [PDF] |
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