Targeting Vascular NADPH Oxidase 1 Blocks Tumor Angiogenesis through a PPARα Mediated Mechanism

Garrido‐Urbani, Sarah; Jemelin, Stéphane; Deffert, Christine; Carnesecchi, Stéphanie; Basset, Olivier; Szyndralewiez, Cédric; Heitz, Freddy; Page, Patrick; Montet, Xavier; Michalik, Liliane; Arbiser, Jack L.; Rüegg, Curzio; Krause, Karl‐Heinz; Imhof, Beat A.

doi:10.1371/journal.pone.0014665

Cited by 132 publications

(136 citation statements)

References 70 publications

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“…The depletion of myelomonocytic cells by inducible diphtheria toxin receptor (LysM iDTR mice) attenuated Ang II-induced blood pressure increase and reduced vascular O 2 -formation (450). Moreover, adoptive transfer of wild-type monocytes into depleted LysM iDTR mice re-established the Ang II-induced oxidative stress, and arterial hypertension, whereas adoptive transfer of neutrophils or monocytes lacking NOX2 did not (129). The NOX2 activity has also been implicated in cardiac inflammation and fibrosis.…”

Section: A Nadph Oxidase-derived Ros In Inflammationmentioning

confidence: 99%

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Reactive Oxygen Species in Inflammation and Tissue Injury

Mittal

Siddiqui

Tran

et al. 2014

Antioxidants & Redox Signaling

3,454

2,424

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Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury. Antioxid. Redox Signal. 20, 1126-1167.

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Section: A Nadph Oxidase-derived Ros In Inflammationmentioning

confidence: 99%

“…NOX1 was also important in angiogenesis and tumor formation. Mice deficient in NOX1 exhibited impaired angiogenesis and tumor growth (129). Activity of NOX1 was increased in endothelial cells on angiogenic stimulation.…”

Section: A Nadph Oxidase-derived Ros In Inflammationmentioning

confidence: 99%

Reactive Oxygen Species in Inflammation and Tissue Injury

Mittal

Siddiqui

Tran

et al. 2014

Antioxidants & Redox Signaling

3,454

2,424

View full text Add to dashboard Cite

show abstract

“…117 When NOX1 is knocked out in a mouse, angiogenic activity is impaired. 120 Likewise, in the NOX2 mouse knockout or when NOX2 is inhibited, ischemia-induced neovascularization is impaired. 119 Though ROS are known to have an important role in ischemic angiogenesis, additional study is required to more specifically determine the role of ROS in delayed HT after ischemic stroke.…”

Section: Delayed Hemorrhagic Transformationmentioning

confidence: 99%

Hemorrhagic Transformation after Ischemic Stroke in Animals and Humans

Jickling

Liu

Stamova

et al. 2013

J Cereb Blood Flow Metab

449

369

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Hemorrhagic transformation (HT) is a common complication of ischemic stroke that is exacerbated by thrombolytic therapy. Methods to better prevent, predict, and treat HT are needed. In this review, we summarize studies of HT in both animals and humans. We propose that early HT (o18 to 24 hours after stroke onset) relates to leukocyte-derived matrix metalloproteinase-9 (MMP-9) and brain-derived MMP-2 that damage the neurovascular unit and promote blood-brain barrier (BBB) disruption. This contrasts to delayed HT (418 to 24 hours after stroke) that relates to ischemia activation of brain proteases (MMP-2, MMP-3, MMP-9, and endogenous tissue plasminogen activator), neuroinflammation, and factors that promote vascular remodeling (vascular endothelial growth factor and high-moblity-group-box-1). Processes that mediate BBB repair and reduce HT risk are discussed, including transforming growth factor beta signaling in monocytes, Src kinase signaling, MMP inhibitors, and inhibitors of reactive oxygen species. Finally, clinical features associated with HT in patients with stroke are reviewed, including approaches to predict HT by clinical factors, brain imaging, and blood biomarkers. Though remarkable advances in our understanding of HT have been made, additional efforts are needed to translate these discoveries to the clinic and reduce the impact of HT on patients with ischemic stroke.

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“…Cet effet est comparable à celui de l'inhibiteur de l'angiogenèse précédemment décrit, l'anticorps anti-VEGFR2 (DC101). Cependant, contrairement au VEGFR2 qui induit l'angiogenèse en activant la voie ERK, les ERO générées par NOX-1 stimulent l'angiogenèse en inactivant le peroxisome proliferator activator receptor-a (PPAR-) qui contrôle l'activité de NF-B, [23] ( Figure 4A). Le mécanisme par lequel les ERO produites par NOX-1 inhibent PPAR- n'est pas encore élucidé.…”

Section: Revuesunclassified

“…NOX-1 sécrète des ERO qui bloquent l'activation du facteur de transcription PPAR-, un inhibiteur de NF-B. Les ERO produites par NOX-1 activent, par conséquent, la migration et l'invasion des cellules endothéliales [23]. B. Dans les cellules tumorales, NOX-4 contribue à la prolifé-ration et à la survie des cellules par l'activation des voies Akt et NF-B.…”

Section: Revuesunclassified