NOX-2S is a new member of the NOX family of NADPH oxidases

Heidari, Yasin; Shah, Ajay M.; Gove, Christopher D.

doi:10.1016/j.gene.2004.03.019

Cited by 10 publications

(7 citation statements)

References 29 publications

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“…In human aortic and corneal endothelial cells, DMSO treatment also did not exert any toxic effect on cells even at the concentrations well above those used in our study [Giovanni et al, ; Camici et al, ]. Moreover, the DMSO concentrations used in our study are also below those used to induce cellular differentiation (1.25%) [Heidari et al, ].…”

Section: Discussionsupporting

confidence: 44%

Dimethyl Sulfoxide Attenuates Hydrogen Peroxide‐Induced Injury in Cardiomyocytes via Heme Oxygenase‐1

Wang

Ding

et al. 2014

J of Cellular Biochemistry

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The antioxidant property of dimethyl sulfoxide (DMSO) was formerly attributed to its direct effects. Our former study showed that DMSO is able to induce heme oxygenase-1 (HO-1) expression in endothelial cells, which is a potent antioxidant enzyme. In this study, we hypothesized that the antioxidant effects of DMSO in cardiomyocytes are mediated or partially mediated by increased HO-1 expression. Therefore, we investigated whether DMSO exerts protective effects against H2 O2 -induced oxidative damage in cardiomyocytes, and whether HO-1 is involved in DMSO-imparted protective effects, and we also explore the underlying mechanism of DMSO-induced HO-1 expression. Our study demonstrated that DMSO pretreatment showed a cytoprotective effect against H2 O2 -induced oxidative damage (impaired cell viability, increased apopototic cells rate and caspase-3 level, and increased release of LDH and CK) and this process is partially mediated by HO-1 upregulation. Furthermore, our data showed that the activation of p38 MAPK and Nrf2 translocation are involved in the HO-1 upregulation induced by DMSO. This study reports for the first time that the cytoprotective effect of DMSO in cardiomyocytes is partially mediated by HO-1, which may further explain the mechanisms by which DMSO exerts cardioprotection on H2 O2 injury. J. Cell. Biochem. 115: 1159-1165, 2014. © 2013 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 44%

Dimethyl Sulfoxide Attenuates Hydrogen Peroxide‐Induced Injury in Cardiomyocytes via Heme Oxygenase‐1

Wang

Ding

et al. 2014

J of Cellular Biochemistry

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“…26 Moreover, DMSO has been routinely used to trigger in vitro cellular differentiation at concentrations as high as 1.25% (15.7 mmol/L). 27 Thus, the DMSO concentrations applied in the present study are clearly below those used to induce cellular differentiation.…”

Section: Discussionmentioning

confidence: 80%

Dimethyl Sulfoxide Inhibits Tissue Factor Expression, Thrombus Formation, and Vascular Smooth Muscle Cell Activation

et al. 2006

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Background-Subacute stent thrombosis is a major clinical concern, and the search for new molecules to cover stents remains important. Dimethyl sulfoxide (DMSO) is used for preservation of hematopoietic progenitor cells and is infused into patients undergoing bone marrow transplantation. Despite its intravenous application, the impact of DMSO on vascular cells has not been assessed. Methods and Results-In human endothelial cells, monocytes, and vascular smooth muscle cells (VSMC), DMSO inhibited tissue factor (TF) expression and activity in response to tumor necrosis factor-␣ or thrombin in a concentration-dependent manner. DMSO did not exert any toxic effects as assessed by phase-contrast microscopy, trypan blue exclusion, and lactate dehydrogenase release. Real-time polymerase chain reaction revealed that inhibition of TF expression occurred at the mRNA level. This effect was mediated by reduced activation of the mitogen-activated protein kinases c-Jun terminal NH 2 kinase (51Ϯ6%; Pϭ0.0005) and p38 (50Ϯ3%; PϽ0.0001) but not p44/42 (PϭNS). In contrast to TF, DMSO did not affect expression of TF pathway inhibitor or plasminogen activator inhibitor-1. In vivo, DMSO treatment suppressed TF activity (41%; PϽ0.002) and prevented thrombotic occlusion in a mouse carotid artery photochemical injury model. DMSO also inhibited VSMC proliferation (70%; Pϭ0.005) and migration (77%; Pϭ0.0001) in a concentration-dependent manner; moreover, it prevented rapamycin and paclitaxel-induced upregulation of TF expression. Conclusions-DMSO suppresses TF expression and activity, as well as thrombus formation; in addition, it inhibits VSMC proliferation and migration. Given its routine use in modern clinical practice, we propose DMSO as a novel strategy for coating drug-eluting stents and treating acute coronary syndromes.

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“…have dominant negative characteristics for ROS generation (116). A novel Nox2 splice variant was also identified which is predicted to give rise to a truncated protein comprising only two transmembrane domains, together with a new Cterminal sequence, although the functional characteristics of this variant have not yet been established (133). A previously described Nox1 splice variant, however, subsequently proved to be an artifact (19,104).…”

Section: Nadph Oxidase Subunit Expression In Cardiovascular Cellsmentioning

confidence: 99%

NADPH Oxidases in Cardiovascular Health and Disease

Cave

Brewer

Narayanapanicker

et al. 2006

Antioxidants & Redox Signaling

576

506

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Increased oxidative stress plays an important role in the pathophysiology of cardiovascular diseases such as hypertension, atherosclerosis, diabetes, cardiac hypertrophy, heart failure, and ischemia-reperfusion. Although several sources of reactive oxygen species (ROS) may be involved, a family of NADPH oxidases appears to be especially important for redox signaling and may be amenable to specific therapeutic targeting. These include the prototypic Nox2 isoform-based NADPH oxidase, which was first characterized in neutrophils, as well as other NADPH oxidases such as Nox1 and Nox4. These Nox isoforms are expressed in a cell- and tissue-specific fashion, are subject to independent activation and regulation, and may subserve distinct functions. This article reviews the potential roles of NADPH oxidases in both cardiovascular physiological processes (such as the regulation of vascular tone and oxygen sensing) and pathophysiological processes such as endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, angiogenesis, and vascular and cardiac remodeling. The complexity of regulation of NADPH oxidases in these conditions may provide the possibility of targeted therapeutic manipulation in a cell-, tissue- and/or pathway-specific manner at appropriate points in the disease process.

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NOX-2S is a new member of the NOX family of NADPH oxidases

Cited by 10 publications

References 29 publications

Dimethyl Sulfoxide Attenuates Hydrogen Peroxide‐Induced Injury in Cardiomyocytes via Heme Oxygenase‐1

Dimethyl Sulfoxide Attenuates Hydrogen Peroxide‐Induced Injury in Cardiomyocytes via Heme Oxygenase‐1

Dimethyl Sulfoxide Inhibits Tissue Factor Expression, Thrombus Formation, and Vascular Smooth Muscle Cell Activation

NADPH Oxidases in Cardiovascular Health and Disease

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