Proteomic characterization of nitrated cell targets after hypobaric hypoxia and reoxygenation in rat brain

Peinado, M.A.; Hernández, Raquel; Peragón, Juan; Ovelleiro, David; Pedrosa, Juan Ángel; Blanco, Santos

doi:10.1016/j.jprot.2014.07.015

Cited by 17 publications

(12 citation statements)

References 88 publications

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“…Thus, during reperfusion, both superoxide and Á NO are available in close proximity for the production of peroxynitrite. The relatively small number of proteins that undergo tyrosyl nitration during experimental hypoxia-reoxygenation [70] is probably a function of the chemical environment/reactivity of the tyrosyl residue.…”

Section: Glutamine Synthetase and Strokementioning

confidence: 99%

“…The protection of glutamine synthesis may reflect the superior defenses of the astrocytes, as compared to neurons, against damaging levels of oxygen-and nitrogen-centered reactive species or the activity of denitrases as discussed earlier. Peinado et al [70] reported increased tyrosyl nitration of cortical glutamine synthetase following hypoxia and reperfusion. The identity of the nitrated tyrosyl residues was not established and therefore may not include Tyr336, which when nitrated inactivates glutamine synthetase [39].…”

Section: Glutamine Synthetase and Strokementioning

confidence: 99%

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Critical Evaluation of the Changes in Glutamine Synthetase Activity in Models of Cerebral Stroke

2015

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The following article addresses some seemingly paradoxical observations concerning cerebral glutamine synthetase in ischemia-reperfusion injury. In the brain, this enzyme is predominantly found in astrocytes and catalyzes part of the glutamine-glutamate cycle. Glutamine synthetase is also thought to be especially sensitive to inactivation by the oxygen- and nitrogen-centered radicals generated during strokes. Despite this apparent sensitivity, glutamine synthetase specific activity is elevated in the affected tissues during reperfusion. Given the central role of the glutamine-glutamate cycle in the brain, we sought to resolve these conflicting observations with the view of providing an alternative perspective for therapeutic intervention in stroke.

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Section: Glutamine Synthetase and Strokementioning

confidence: 99%

Section: Glutamine Synthetase and Strokementioning

confidence: 99%

Critical Evaluation of the Changes in Glutamine Synthetase Activity in Models of Cerebral Stroke

2015

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“…1E). Therefore, additional formation of NO from L-arginine (that we previously proved with atomic force microscopy [8] ), did not contributed to activation of SC migration processes in hippocampus that could probably happen due to double role of NO in brain: adjusting character on the one hand and -on the other hand -peroxynitrite formation that activates protective mechanisms against hypoxia in the organism including initiation of SC migration processes [9,10] .…”

Section: Resultsmentioning

confidence: 76%

“…However, single SC began appearing in hippocampal tissue near GD that hypothetically indicated SC movement towards damaged regions at hippocampal edges. The fact of SC movement towards damaged zones of nerve tissue is known [6,9,11] , and experimentally proved in vivo [12,13] . Performed in vitro investigation presents evidence for location and movement of SC in survival hippocampal slices.…”

Section: Resultsmentioning

confidence: 99%

Migration of Neural Stem Cells in Hippocampal Slices in Hypoxia Modeling

Stukach¹,

Gainutdinov²,

Dosina³

et al. 2017

JSCRT

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“…Proteomic analysis revealed that nitration-related proteins included metabolism proteins, cytoskeleton proteins, chaperones and carrier proteins in the samples from hypoxia/reoxygenated brain tissues. [166] About 23 proteins tyrosine nitration were identified in I/R heart and 10 of them were from mitochondria. [167] Interestingly, mitochondrial proteins appear to be more susceptible to nitration stress.…”

Section: Rns-mediated Autophagy/mitophagy Under Ischemia Insultmentioning

confidence: 99%

Reactive nitrogen species as therapeutic targets for autophagy: implication for ischemic stroke

Feng

Chen

Shen

2017

Expert Opinion on Therapeutic Targets

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Roles of autophagy/mitophagy activation in ischemic stroke remain controversial. To elucidate potential reasons, we analyze the factors responsible for divergent results in literatures. Reactive nitrogen species (RNS) are important cytotoxic factors in ischemic stroke. Herein, we particularly discuss the roles played by RNS in autophagy/mitophagy and ischemic brain injury. Areas covered: Following factors should be considered in the studies on autophagy/mitophagy in ischemic stroke: (1) Protocols for administration of autophagy regulators including administration time points, routes and doses, etc.; (2) Specificity of autophagy regulators; (3) Animal models of cerebral ischemia with or without reperfusion. In the underlying mechanisms of autophagy/mitophagy, we particularly discuss the potential roles of RNS in mediating excessive autophagy/mitophagy during cerebral ischemia/reperfusion injury. Expert opinion: Emphasis should be given to the following aspects in future studies: (1) Targeting RNS and related cellular signaling pathways in the regulation of autophagy/mitophagy might be a promising strategy for developing novel drugs as well as combined therapy for thrombolytic treatment to reach better outcomes for ischemic stroke; (2) Developing circulating plasma biomarkers linking RNS-mediated autophagy/mitophagy to the magnitude of ischemic brain injury will benefit for stroke treatment. Subsequently, RNS could be dominant therapeutic targets to regulate autophagy/mitophagy for ischemic stroke.

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Proteomic characterization of nitrated cell targets after hypobaric hypoxia and reoxygenation in rat brain

Cited by 17 publications

References 88 publications

Critical Evaluation of the Changes in Glutamine Synthetase Activity in Models of Cerebral Stroke

Critical Evaluation of the Changes in Glutamine Synthetase Activity in Models of Cerebral Stroke

Migration of Neural Stem Cells in Hippocampal Slices in Hypoxia Modeling

Reactive nitrogen species as therapeutic targets for autophagy: implication for ischemic stroke

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