Role of Cyclooxygenase and Derived Reactive Oxygen Species in ρ-Kinase-Mediated Impairment of Endothelium-Dependent Vasodilation and Blood Flow after Ischemia-Reperfusion of the Rat Kidney

2010 ◽  
Vol 114 (1) ◽  
pp. e1-e6 ◽  
Author(s):  
Amanda M.G. Versteilen ◽  
Iolente J.M. Korstjens ◽  
René J.P. Musters ◽  
A.B. Johan Groeneveld ◽  
Pieter Sipkema
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Flow ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Rho Kinase ◽  
Reactive Oxygen ◽  
Oxygen Species

The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

2020 ◽  
Vol 16 ◽  
Author(s):  
Andrey Krylatov ◽  
Leonid Maslov ◽  
Sergey Y. Tsibulnikov ◽  
Nikita Voronkov ◽  
Alla Boshchenko ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Hydrogen Sulfide ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Ischemia And Reperfusion Injury ◽  
Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

ROLE OF MITOCHONDRIAL NITRIC OXIDE AND REACTIVE OXYGEN SPECIES IN RAT KIDNEY DURING DIABETES

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Edgar Esquivel‐Gutiérrez ◽  
Ruth Noriega‐Cisneros ◽  
Mónica Clemente‐Guerrero ◽  
Evangelina Caudillo‐Noriega ◽  
Areli Gutiérrez‐Pérez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Rat Kidney ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Attenuation of Ischemia-Induced Mouse Brain Injury by SAG, a Redox-Inducible Antioxidant Protein

2001 ◽  
Vol 21 (6) ◽  
pp. 722-733 ◽  
Author(s):  
Guo-Yuan Yang ◽  
Li Pang ◽  
Hai-Liang Ge ◽  
Mingjia Tan ◽  
Wen Ye ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Brain Injury ◽  
Mouse Brain ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Model Systems ◽  
Oxygen Species ◽  
Antioxidant Protein

Cerebral ischemia resulting from a disruption of blood flow to the brain initiates a cascade of events that causes neuron death and leads to neurologic dysfunction. Reactive oxygen species are thought, at least in part, to mediate this disease process. The authors recently cloned and characterized an antioxidant protein, SAG (sensitive to apoptosis gene), that is redox inducible and protects cells from apoptosis induced by redox agents in a number of in vitro cell model systems. This study reports a neuroprotective role of SAG in ischemia/reperfusion-induced brain injury in an in vivo mouse model. SAG was expressed at a low level in brain tissue and was inducible after middle cerebral artery occlusion with peak expression at 6 to 12 hours. At the cellular level, SAG was mainly expressed in the cytoplasm of neurons and astrocytes, revealed by double immunofluorescence. An injection of recombinant adenoviral vector carrying human SAG into mouse brain produced an overexpression of SAG protein in the injected areas. Transduction of AdCMVSAG (wild-type), but not AdCMVmSAG (mutant), nor the AdCMVlacZ control, protected brain cells from ischemic brain injury, as evidenced by significant reduction of the infarct areas where SAG was highly expressed. The result suggests a rather specific protective role of SAG in the current in vivo model. Mechanistically, SAG overexpression decreased reactive oxygen species production and reduced the number of apoptotic cells in the ischemic areas. Thus, antioxidant SAG appears to protect against reactive oxygen species–induced brain damage in mice. Identification of SAG as a neuroprotective molecule could lead to potential stroke therapies.

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