scholarly journals Pigment Epithelium-Derived Factor Inhibits Neointimal Hyperplasia after Vascular Injury by Blocking NADPH Oxidase-Mediated Reactive Oxygen Species Generation

2007 ◽  
Vol 170 (6) ◽  
pp. 2159-2170 ◽  
Author(s):  
Kazuo Nakamura ◽  
Sho-ichi Yamagishi ◽  
Takanori Matsui ◽  
Takafumi Yoshida ◽  
Katsuhiko Takenaka ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Vascular Injury ◽  
Pigment Epithelium ◽  
Neointimal Hyperplasia ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Pigment Epithelium Derived Factor

scholarly journals The Involvement of the Tyrosine Kinase c-Src in the Regulation of Reactive Oxygen Species Generation Mediated by NADPH Oxidase-1

2008 ◽  
Vol 19 (7) ◽  
pp. 2984-2994 ◽  
Author(s):  
Davide Gianni ◽  
Ben Bohl ◽  
Sara A. Courtneidge ◽  
Gary M. Bokoch
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Tyrosine Kinase ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Tumor Formation ◽  
Ros Generation ◽  
Oxygen Species ◽  
Human Colon Carcinoma Cell ◽  
Kinase C

NADPH oxidase (Nox) family enzymes are one of the main sources of cellular reactive oxygen species (ROS), which have been shown to function as second messenger molecules. To date, seven members of this family have been reported, including Nox1-5 and Duox1 and -2. With the exception of Nox2, the regulation of the Nox enzymes is still poorly understood. Nox1 is highly expressed in the colon, and it requires two cytosolic regulators, NoxO1 and NoxA1, as well as the binding of Rac1 GTPase, for its activity. In this study, we investigate the role of the tyrosine kinase c-Src in the regulation of ROS formation by Nox1. We show that c-Src induces Nox1-mediated ROS generation in the HT29 human colon carcinoma cell line through a Rac-dependent mechanism. Treatment of HT29 cells with the Src inhibitor PP2, expression of a kinase-inactive form of c-Src, and c-Src depletion by small interfering RNA (siRNA) reduce both ROS generation and the levels of active Rac1. This is associated with decreased Src-mediated phosphorylation and activation of the Rac1-guanine nucleotide exchange factor Vav2. Consistent with this, Vav2 siRNA that specifically reduces endogenous Vav2 protein is able to dramatically decrease Nox1-dependent ROS generation and abolish c-Src-induced Nox1 activity. Together, these results establish c-Src as an important regulator of Nox1 activity, and they may provide insight into the mechanisms of tumor formation in colon cancers.

scholarly journals Essential Role of NADPH Oxidase-Dependent Reactive Oxygen Species Generation in Regulating MicroRNA-21 Expression and Function in Prostate Cancer

2013 ◽  
Vol 19 (16) ◽  
pp. 1863-1876 ◽  
Author(s):  
Sarvesh Jajoo ◽  
Debashree Mukherjea ◽  
Tejbeer Kaur ◽  
Kelly E. Sheehan ◽  
Sandeep Sheth ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Essential Role ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
And Function

scholarly journals The Protective Effect of Ubiquinone against the Amyloid Peptide in Endothelial Cells Is Isoprenoid Chain Length-Dependent

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1806
Author(s):  
Javier Frontiñán-Rubio ◽  
Yoana Rabanal-Ruiz ◽  
Mario Durán-Prado ◽  
Francisco Javier Alcain
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Nadph Oxidase ◽  
Protective Effect ◽  
Vascular Dysfunction ◽  
Reactive Oxygen Species Generation ◽  
Density Lipoprotein ◽  
Reactive Oxygen ◽  
Amyloid Peptide ◽  
Oxygen Species

Vascular brain pathology constitutes a common feature in neurodegenerative diseases that could underlie their development. Indeed, vascular dysfunction acts synergistically with neurodegenerative changes to exacerbate the cognitive impairment found in Alzheimer’s disease. Different injuries such as hypertension, high glucose, atherosclerosis associated with oxidized low-density lipoprotein or inflammation induce NADPH oxidase activation, overproduction of reactive oxygen species, and apoptosis in endothelial cells. Since it has been shown that pretreatment of cultured endothelial cells with the lipophilic antioxidant coenzyme Q10 (CoQ10) displays a protective effect against the deleterious injuries caused by different agents, this study explores the cytoprotective role of different CoQs homologues against Aβ25–35-induced damage and demonstrates that only pretreatment with CoQ10 protects endothelial brain cells from Aβ25–35-induced damage. Herein, we show that CoQ10 constitutes the most effective ubiquinone in preventing NADPH oxidase activity and reducing both reactive oxygen species generation and the increase in free cytosolic Ca2+ induced by Aβ25–35, ultimately preventing apoptosis and necrosis. The specific cytoprotective effect of CoQ with a side chain of 10 isoprenoid units could be explained by the fact that CoQ10 is the only ubiquinone that significantly reduces the entry of Aβ25–35 into the mitochondria.

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