2006
DOI: 10.1161/01.str.0000221708.17159.64
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Potential Contribution of NF-κB in Neuronal Cell Death in the Glutathione Peroxidase-1 Knockout Mouse in Response to Ischemia-Reperfusion Injury

Abstract: Background and Purpose-We have previously identified an increased susceptibility of Gpx1 Ϫ/Ϫ mice to increased infarct size after middle cerebral artery occlusion (MCAO). This study was designed to elucidate the mechanisms involved in elevated neuronal cell death arising from an altered endogenous oxidant state. Methods-Gpx1Ϫ/Ϫ mice were exposed to transient MCAO and reperfusion by intraluminal suture blockade. Protein expression of the p65 subunit of transcription factor nuclear factor-B (NF-B) was examined b… Show more

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Cited by 83 publications
(64 citation statements)
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“…The absence of a significant ischemia-induced increase in NFκB activation is in contrast to findings from the majority of experimental global and focal brain ischemia studies [5,[7][8][9][10][11][12][13][14]. Our result is most likely accounted for by the inconsistent ischemic severity demonstrated in our model.…”
Section: Discussioncontrasting
confidence: 99%
See 1 more Smart Citation
“…The absence of a significant ischemia-induced increase in NFκB activation is in contrast to findings from the majority of experimental global and focal brain ischemia studies [5,[7][8][9][10][11][12][13][14]. Our result is most likely accounted for by the inconsistent ischemic severity demonstrated in our model.…”
Section: Discussioncontrasting
confidence: 99%
“…Nuclear factor κB (NFκB) is a transcription factor that is key in amplifying the inflammatory response involved in stroke pathophysiology [3,4]. Increased NFκB activation has been demonstrated in human stroke [5,6] and experimental models of brain ischemia [5,[7][8][9][10][11][12][13][14].…”
Section: Introductionmentioning
confidence: 99%
“…Total and nuclear extracts were prepared essentially according to Crack et al (2006), except that 1ϫ protease inhibitor cocktail (Roche Applied Science) was added to the buffers used and that protein concentrations were estimated using the Qubit Protein Assay according to the manufacturer (Invitrogen). Western blot analysis was performed using 25 and 50 g of nuclear extract and supernatant, respectively, separated on 10% SDS-PAGE gels.…”
Section: Methodsmentioning
confidence: 99%
“…Extracellular stimuli that activate the NF-κB pathway include proinflammatory cytokines, physical and oxidative stress, apoptotic mediators, elevation of intracellular calcium levels and excitotoxicity (Barnes and Karin, 1997;Ghosh et al, 1998;Siebenlist et al, 1994), many of which have been implicated in pathogenesis of post-ischemic injury (Crack et al, 2006;Herrmann et al, 2005;Nurmi et al, 2004;Schneider et al, 1999). In severe ischemia, NF-κB contributes to neuronal cell death program leading to irreversible brain damage.…”
Section: Nf-κb and Strokementioning
confidence: 99%
“…We afforded the dual effect of NF-κB activation in preconditioning and lethal ischemia using neuronal cells exposed to oxygen glucose deprivation (OGD) and mice subjected to middle cerebral artery occlusion (MCAO) (Lanzillotta et al, 2010;Pizzi et al, 2009). After exposure to lethal ischemia, neuronal nuclei displayed a high level of p50/RelA activation (Crack et al, 2006;Inta et al, 2006) and decreased level of c-Relcontaining dimers (Sarnico et al, 2009a(Sarnico et al, , 2009b. Accordingly, mice deficient in p50 or RelA, but not mice deficient in c-Rel subunit, showed a reduced infarct size when exposed to MCAO (Inta et al, 2006;Schneider et al, 1999).…”
Section: Nf-κb and Strokementioning
confidence: 99%