scholarly journals NADPH oxidase 5 (NOX5)-induced reactive oxygen signaling modulates normoxic HIF-1α and p27Kip1 expression in malignant melanoma and other human tumors

2017 ◽  
Vol 56 (12) ◽  
pp. 2643-2662 ◽  
Author(s):  
Smitha Antony ◽  
Guojian Jiang ◽  
Yongzhong Wu ◽  
Jennifer L. Meitzler ◽  
Hala R. Makhlouf ◽  
...  
Keyword(s):  
Malignant Melanoma ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Human Tumors ◽  
P27kip1 Expression ◽  
Oxygen Signaling ◽  
Nadph Oxidase 5

Abstract 4796: Characterization of NADPH oxidase 5 expression in human tumors and tumor cell lines with a novel mouse monoclonal antibody.

2013 ◽  
Author(s):  
Smitha Antony ◽  
Yongzhong Wu ◽  
Stephen M. Hewitt ◽  
Miriam R. Anver ◽  
Guojian Jiang ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Nadph Oxidase ◽  
Tumor Cell ◽  
Cell Lines ◽  
Human Tumors ◽  
Mouse Monoclonal Antibody ◽  
Tumor Cell Lines ◽  
Nadph Oxidase 5

Human monocytes and macrophages express NADPH oxidase 5; a potential source of reactive oxygen species in atherosclerosis

2015 ◽  
Vol 461 (1) ◽  
pp. 172-179 ◽  
Author(s):  
Adrian Manea ◽  
Simona-Adriana Manea ◽  
Ana Maria Gan ◽  
Alina Constantin ◽  
Ioana Madalina Fenyo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Human Monocytes ◽  
Potential Source ◽  
Monocytes And Macrophages ◽  
Human Monocytes And Macrophages ◽  
Nadph Oxidase 5

scholarly journals Ca 2+ -Dependent NOX5 (NADPH Oxidase 5) Exaggerates Cardiac Hypertrophy Through Reactive Oxygen Species Production

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 827-838 ◽  
Author(s):  
Guo-Jun Zhao ◽  
Chang-Ling Zhao ◽  
Shan Ouyang ◽  
Ke-Qiong Deng ◽  
Lihua Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Cardiac Hypertrophy ◽  
Reactive Oxygen ◽  
Contractile Dysfunction ◽  
Oxygen Species ◽  
Ang Ii ◽  
Rat Cardiomyocytes ◽  
Nadph Oxidase 5

NOX5 (NADPH oxidase 5) is a homolog of the gp91 phox subunit of the phagocyte NOX, which generates reactive oxygen species. NOX5 is involved in sperm motility and vascular contraction and has been implicated in diabetic nephropathy, atherosclerosis, and stroke. The function of NOX5 in the cardiac hypertrophy is unknown. Because NOX5 is a Ca 2+ -sensitive, procontractile NOX isoform, we questioned whether it plays a role in cardiac hypertrophy. Studies were performed in (1) cardiac tissue from patients undergoing heart transplant for cardiomyopathy and heart failure, (2) NOX5-expressing rat cardiomyocytes, and (3) mice expressing human NOX5 in a cardiomyocyte-specific manner. Cardiac hypertrophy was induced in mice by transverse aorta coarctation and Ang II (angiotensin II) infusion. NOX5 expression was increased in human failing hearts. Rat cardiomyocytes infected with adenoviral vector encoding human NOX5 cDNA exhibited elevated reactive oxygen species levels with significant enlargement and associated increased expression of ANP (atrial natriuretic peptides) and β-MHC (β-myosin heavy chain) and prohypertrophic genes ( Nppa , Nppb , and Myh7 ) under Ang II stimulation. These effects were reduced by N-acetylcysteine and diltiazem. Pressure overload and Ang II infusion induced left ventricular hypertrophy, interstitial fibrosis, and contractile dysfunction, responses that were exaggerated in cardiac-specific NOX5 trangenic mice. These phenomena were associated with increased reactive oxygen species levels and activation of redox-sensitive MAPK (mitogen-activated protein kinase). N-acetylcysteine treatment reduced cardiac oxidative stress and attenuated cardiac hypertrophy in NOX5 trangenic. Our study defines Ca 2+ -regulated NOX5 as an important NOX isoform involved in oxidative stress- and MAPK-mediated cardiac hypertrophy and contractile dysfunction.

scholarly journals Characterization of NADPH oxidase 5 expression in human tumors and tumor cell lines with a novel mouse monoclonal antibody

2013 ◽  
Vol 65 ◽  
pp. 497-508 ◽  
Author(s):  
Smitha Antony ◽  
Yongzhong Wu ◽  
Stephen M. Hewitt ◽  
Miriam R. Anver ◽  
Donna Butcher ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Nadph Oxidase ◽  
Tumor Cell ◽  
Cell Lines ◽  
Human Tumors ◽  
Mouse Monoclonal Antibody ◽  
Tumor Cell Lines ◽  
Nadph Oxidase 5

scholarly journals Role of NADPH Oxidase-Mediated Reactive Oxygen Species in Podocyte Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Shan Chen ◽  
Xian-Fang Meng ◽  
Chun Zhang
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Epithelial To Mesenchymal Transition ◽  
Kidney Diseases ◽  
Treatment Strategies ◽  
Reactive Oxygen ◽  
Glomerular Sclerosis ◽  
Oxygen Species ◽  
Podocyte Injury ◽  
Mesenchymal Transition

Proteinuria is an independent risk factor for end-stage renal disease (ESRD) (Shankland, 2006). Recent studies highlighted the mechanisms of podocyte injury and implications for potential treatment strategies in proteinuric kidney diseases (Zhang et al., 2012). Reactive oxygen species (ROS) are cellular signals which are closely associated with the development and progression of glomerular sclerosis. NADPH oxidase is a district enzymatic source of cellular ROS production and prominently expressed in podocytes (Zhang et al., 2010). In the last decade, it has become evident that NADPH oxidase-derived ROS overproduction is a key trigger of podocyte injury, such as renin-angiotensin-aldosterone system activation (Whaley-Connell et al., 2006), epithelial-to-mesenchymal transition (Zhang et al., 2011), and inflammatory priming (Abais et al., 2013). This review focuses on the mechanism of NADPH oxidase-mediated ROS in podocyte injury under different pathophysiological conditions. In addition, we also reviewed the therapeutic perspectives of NADPH oxidase in kidney diseases related to podocyte injury.

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