Ethanol-induced erectile dysfunction and increased expression of pro-inflammatory proteins in the rat cavernosal smooth muscle are mediated by NADPH oxidase-derived reactive oxygen species

2017 ◽  
Vol 804 ◽  
pp. 82-93 ◽  
Author(s):  
Letícia N. Leite ◽  
Gabriel T. do Vale ◽  
Janaina A. Simplicio ◽  
Bruno S. De Martinis ◽  
Fernando S. Carneiro ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Smooth Muscle ◽  
Erectile Dysfunction ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Inflammatory Proteins

scholarly journals Reactive oxygen species and erectile dysfunction: possible role of NADPH oxidase

2006 ◽  
Vol 19 (3) ◽  
pp. 265-280 ◽  
Author(s):  
J Y Jeremy ◽  
R A Jones ◽  
A J Koupparis ◽  
M Hotston ◽  
R Persad ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Erectile Dysfunction ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Reactive Oxygen Species from NADPH Oxidase and Mitochondria Participate in the Proliferation of Aortic Smooth Muscle Cells from a Model of Metabolic Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Ocarol López-Acosta ◽  
María de los Angeles Fortis-Barrera ◽  
Miguel Angel Barrios-Maya ◽  
Angélica Ruiz Ramírez ◽  
Francisco Javier Alarcón Aguilar ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
Smooth Muscle ◽  
Cell Growth ◽  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Metabolic Diseases ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
And Control

In metabolic diseases, the increased reactive oxygen species (ROS) represents one of the pathogenic mechanisms for vascular disease probably by promoting vascular smooth muscle cell (SMC) proliferation that contributes to the development of arterial remodeling and stenosis, hypertension, and atherosclerosis. Therefore, this work was undertaken to evaluate the participation of ROS from NADPH oxidase and mitochondria in the proliferation of SMCs from the aorta in a model of metabolic syndrome induced by sucrose feeding in rats. After 24 weeks, sucrose-fed (SF) rats develop hypertension, intra-abdominal obesity, hyperinsulinemia, and hyperleptinemia. In addition SMCs from SF rats had a higher growth rate and produce more ROS than control cells. The treatment of SMCs with DPI and apocynin to inhibit NADPH oxidase and with tempol to scavenge superoxide anion significantly blocked the proliferation of both SF and control cells suggesting the participation of NADPH oxidase as a source of superoxide anion. MitoTEMPO, which targets mitochondria within the cell, also significantly inhibited the proliferation of SMCs having a greater effect on cells from SF than from the control aorta. The higher rate of cell growth from the SF aorta is supported by the increased content of cyclophilin A and CD147, proteins involved in the mechanism of cell proliferation. In addition, caldesmon, α-actin, and phosphorylated myosin light chain, contractile phenotype proteins, were found significantly lower in SF cells in no confluent state and increased in confluent state but without difference between both cell types. Our results suggest that ROS from NADPH oxidase and mitochondria significantly participate in the difference found in the rate of cell growth between SF and control cells.

scholarly journals Effects of Lonomia obliqua Venom on Vascular Smooth Muscle Cells: Contribution of NADPH Oxidase-Derived Reactive Oxygen Species

Toxins ◽  
2017 ◽  
Vol 9 (11) ◽  
pp. 360 ◽  
Author(s):  
João Moraes ◽  
Genilson Rodrigues ◽  
Vany Nascimento-Silva ◽  
Mariana Renovato-Martins ◽  
Markus Berger ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Nadph Oxidase ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Reactive Oxygen ◽  
Muscle Cells ◽  
Oxygen Species ◽  
Lonomia Obliqua

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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