This SuperSeries is composed of the SubSeries listed below.
A global transcriptomic view of the multifaceted role of glutathione peroxidase-1 in cerebral ischemic-reperfusion injury.
Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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Sex, Treatment
View SamplesIschemic stroke triggers severe focal hypoperfusion accompanied with deprivation of oxygen and glucose to the cerebral tissue, together with loss of ATP, depolorization of neurons, elevated extracellular potassium concentration, and subsequently leads to excitotoxicity as well as increased oxidative stress promoting microvascular injury, blood-brain-barrier deregulation, post-ischemic inflammation and eventually the consequential neurological deficit. Although reperfusion of ischemic brain tissue is critical for restoring normal function, it can paradoxically result in secondary damage, called ischemia/reperfusion (I/R) injury.
A global transcriptomic view of the multifaceted role of glutathione peroxidase-1 in cerebral ischemic-reperfusion injury.
Treatment
View SamplesGlutathione peroxidase (Gpx) is a selenium-containing enzyme that catalyses the reduction of a variety of biological peroxides at the expense of reduced glutathione (GSH). Gpx1 is the most abundant isoform and its role has been implicated in neurodegenerative disorders such as Parkinsons disease (PD), dementia with Lewy bodies tissue (DLB) (Power and Blumbergs, 2009) and traumatic brain injury (Tsuru-Aoyagi et al., 2009). Due to its high abundance, mutation of the Gpx1 allele would lower overall Gpx activity in the brain significantly. Gpx1 knockout (Gpx1-/-) mice do not show overt phenotypic differences, but all indications suggest that these mice are in a chronic pro-oxidant state (Cheng et al. 1999; de Haan et al. 2004). Indeed, a recent study from our laboratory illustrated that the absence of Gpx1 exacerbated stroke injury via increased ROS production and vascular permeability (Wong et al. 2008). Furthermore, Gpx1-/- mice demonstrated an increase in caspase-3 activation and greater infarct volume (Crack et al. 2001)
No associated publication
Treatment
View SamplesFocal ischemia is triggered by the sudden significant reduction of blood supply to the brain, as a result of either the rupture or occlusion by thrombus/embolism of a blood vessel in the brain. Permanent focal ischemia occurred when blood supply to a specific part of the brain is impeded without reperfusion. Despite major steps achieved in the elucidation of the patho-physiology of cerebral ischemia, the available therapeutic avenues for acute ischemic stroke remain scarce. Cell cycle re-activation has been revealed as a novel signaling pathway during permanent focal ischemia. As such, non-specific aurora kinase inhibitor ZM447439, has been injected intracranial-ventricularly30min post-ischemia induction to determine its efficacy in reduction of neuronal damage in terms of infarct volume.
No associated publication
Sex, Treatment
View SamplesHydrogen sulfide (H2S), present in abundance in the mammalian brain, has recently been demonstrated to induce a dose- and time-dependent apoptotic-necrotic continuum in murine primary cortical neurons, which was successfully attenuated upon application of N-methyl-D-aspartate (NMDA) receptor antagonist. The current study focused on gaining an insight into the molecular mechanisms of H2Smediated neuronal death pertaining to NMDA receptors activation through global gene expression comparisons.
Gene profiling reveals hydrogen sulphide recruits death signaling via the N-methyl-D-aspartate receptor identifying commonalities with excitotoxicity.
Specimen part, Treatment
View SamplesGlutamate, a major neurotransmitter in the mammalian nervous sytem, has been involved in the mediation of excitotoxicity commonly observed in the pathogenesis of stroke. Current study focused on gaining an insight into the molecular mechanisms of glutamate-induced neuronal death
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Specimen part, Time
View SamplesNitric oxide (NO) is implicated in the pathogenesis of various neuropathologies characterised by oxidative stress. NO has been reported to be involved in the exacerbation of oxidative stress by various mechanisms, including protein modification, genotoxic damage and elevated production of reactive oxygen species resulting in deregulation and disruption of cellular homeostasis.
No associated publication
Specimen part, Time
View SamplesInhibition of proteasome degradation pathway has been implicated in neuronal cell death leading to neurodegenerative diseases such as Parkinsons disease and Alzheimers disease. Pharmacological proteasomal inhibitors such as lactacystin can induce apoptosis in cultured mouse cortical neurons through the activation of caspase-3. Furthermore, proteasomal inhibitors are also reported to mediate deleterious alterations in cell cycle regulation, inflammatory processes and protein aggregation and trigger the cell death pathway.
Up-regulation of endoplasmic reticulum stress-related genes during the early phase of treatment of cultured cortical neurons by the proteasomal inhibitor lactacystin.
Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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Sex, Age, Treatment, Race
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