Measurement of striatal H2O2 by microdialysis following global forebrain ischemia and reperfusion in the rat: correlation with the cytotoxic potential of H2O2 in vitro

Hyslop, Paul A.; Zhang, Zhiyuan; Pearson, D; Phebus, Lee A.

doi:10.1016/0006-8993(94)01291-o

Cited by 321 publications

(233 citation statements)

References 23 publications

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“…We then investigated the mechanism by which Ngb inhibited caspase-3 activation. 14-3-3 proteins exist predominantly in the brain and mediate essential apoptotic signaling pathways [28,29] . We have previously reported that 14-3-3γ is up-regulated and protects astrocytes from ischemia-induced apoptosis [24,25] .…”

Section: Resultsmentioning

confidence: 99%

“…An interesting finding is that the silencing of Ngb increases cell death with lower concentrations (150 and 300 µmol/L) but not higher concentrations (450 and 600 µmol/L) of H 2 O 2 . As estimated by microdialysis in the ischemic striatum, the concentration of H 2 O 2 can rise as high as 100 µmol/L during the reperfusion phase [29] . Our data supports a physiological or pathological role of endogenous Ngb in protecting cells from oxidative stress in the central nervous system.…”

Section: Discussionmentioning

confidence: 99%

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Silencing neuroglobin enhances neuronal vulnerability to oxidative injury by down-regulating 14-3-3γ

Zhou

Lai

et al. 2009

Acta Pharmacol Sin

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Aim: To explore the protective role and mechanism of endogenous neuroglobin (Ngb) in neuronal cells under oxidative stress. Methods: A stable N2a neuroblastoma cell line expressing the Ngb-siRNA plasmid (N2a/Ngb-siRNA) was established by neomycin screening. Reverse transcription (RT)-PCR and Western blot analysis were used to detect Ngb gene and protein levels. Hydrogen peroxide was used to induce oxidative stress in N2a cells. Cytotoxicity and cell viability were measured by lactate dehydrogenase (LDH) and WST-8 assays. Hoechst staining demonstrated that the quantity of apoptotic cells among N2a/Ngb-siRNA cells following hydrogen peroxide treatment significantly increased compared with controls. In N2a/Ngb-siRNA cells, the expression level of activated caspase-3 significantly increased, whereas the expression of 14-3-3γ decreased compared with that of N2a/vec cells. Transfection of 14-3-3γ plasmids significantly enhanced the viability of N2a/Ngb-siRNA cells following hydrogen peroxide treatment compared with vector controls. Conclusion: Ngb contributes to neuronal defensive machinery against oxidative injuries by regulating 14-3-3γ expression.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Silencing neuroglobin enhances neuronal vulnerability to oxidative injury by down-regulating 14-3-3γ

Zhou

Lai

et al. 2009

Acta Pharmacol Sin

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“…Some studies have suggested that oxidative damage may be involved in triggering increased cPLA2 activity after ischemia (Hyslop et a!., 1995;Dan et al, 1996). Levels of H2O2 are increased significantly in vulnerable brain regions of animals with ischemic injury.…”

Section: Pla2 and Neurodegenerationmentioning

confidence: 99%

Phospholipase A₂ and Its Role in Brain Tissue

Farooqui

Yang

Rosenberger

et al. 1997

Journal of Neurochemistry

324

202

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Phospholipase A2 (PLA2) is the name for the class of lipolytic enzymes that hydrolyze the acyl group from the sn-2 position of glycerophospholipids, generating free fatty acids and lysophospholipids. The products of the PLA2-catalyzed reaction can potentially act as second messengers themselves, or be further metabolized to eicosanoids, platelet-activating factor, and lysophosphatidic acid. All of these are recognized as bioactive lipids that can potentially alter many ongoing cellular processes. The presence of PLA2 in the central nervous system, accompanied by the relatively large quantity of potential substrate, poses an interesting dilemma as to the role PLAS has during both physiologic and pathologic states. Several different PLA2 enzymes exist in brain, some of which have been partially characterized. They are classified into two subtypes, Ca 2~-dependentand Ca2-independent, based on their catalytic dependence on Ca~.Under physiologic conditions, PLA 2 may be involved in phospholipid turnover, membrane remodeling, exocytosis, detoxification of phospholipid peroxides, and rieurotransmitter release. However, under pathological situations, increased PLA2 activity may result in the loss of essential membrane glycerophospholipids, resulting in altered membrane permeability, ion homeostasis, increased free fatty acid release, and the accumulation of lipid peroxides. These processes, along with loss of ATP, may be responsible for the loss of membrane phospholipid and subsequent neuronal injury found in ischemia, spinal cord injury, and other neurodegenerative diseases. This review outlines the current knowledge of the PLA2 found in the central nervous system and attempts to define the role of PLA2 during both physiologic and pathologic conditions.

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“…H 2 O 2 was reported to be present in 100 lM concentration in the striatum during reperfusion following an ischemic period (Hyslop et al 1995). Unlike the effect of veratridine, that of the H 2 O 2 -induced oxidative stress on the release of glutamate appears to be ambiguous.…”

mentioning

confidence: 99%

Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Tretter

Ádám-Vizi

2002

Journal of Neurochemistry

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Measurement of striatal H2O2 by microdialysis following global forebrain ischemia and reperfusion in the rat: correlation with the cytotoxic potential of H2O2 in vitro

Cited by 321 publications

References 23 publications

Silencing neuroglobin enhances neuronal vulnerability to oxidative injury by down-regulating 14-3-3γ

Silencing neuroglobin enhances neuronal vulnerability to oxidative injury by down-regulating 14-3-3γ

Phospholipase A₂ and Its Role in Brain Tissue

Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

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Measurement of striatal H2O2 by microdialysis following global forebrain ischemia and reperfusion in the rat: correlation with the cytotoxic potential of H2O2 in vitro

Cited by 321 publications

References 23 publications

Silencing neuroglobin enhances neuronal vulnerability to oxidative injury by down-regulating 14-3-3γ

Silencing neuroglobin enhances neuronal vulnerability to oxidative injury by down-regulating 14-3-3γ

Phospholipase A2 and Its Role in Brain Tissue

Glutamate release by an Na+ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Contact Info

Product

Resources

About

Phospholipase A₂ and Its Role in Brain Tissue

Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion