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accession-icon GSE23163
Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo mouse model.
  • organism-icon Mus musculus
  • sample-icon 38 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A global transcriptomic view of the multifaceted role of glutathione peroxidase-1 in cerebral ischemic-reperfusion injury.

Sample Metadata Fields

Treatment

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accession-icon GSE25676
Global gene regulation in permanent focal ischemia in an in vivo rat model
  • organism-icon Rattus norvegicus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE23160
Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo wild-type mouse model.
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Ischemic 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.

Publication Title

A global transcriptomic view of the multifaceted role of glutathione peroxidase-1 in cerebral ischemic-reperfusion injury.

Sample Metadata Fields

Treatment

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accession-icon GSE23162
Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo Gpx1 -/- transgenic mouse model.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Glutathione 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)

Publication Title

No associated publication

Sample Metadata Fields

Treatment

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accession-icon GSE23651
Global transcriptomic profiling of permanent focal ischemia in an in vivo rat model
  • organism-icon Rattus norvegicus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

Focal 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.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE16035
Global gene profiling comparison between hydrogen sulfide- and N-methyl-D-aspartate-induced neuronal deaths
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina MouseRef8 Ver1.1

Description

Hydrogen 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.

Publication Title

Gene profiling reveals hydrogen sulphide recruits death signaling via the N-methyl-D-aspartate receptor identifying commonalities with excitotoxicity.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE19936
Global gene profiling of glutamate-induced neuronal death
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina mouseRef-8 v1.1 expression beadchip

Description

Glutamate, 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

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE22087
Global transcriptomic profiling of nitric oxide-mediated neuronal death
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Nitric 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.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE22465
Global transcriptomic profiling of lactacystin-mediated neuronal death
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Array (mgu74a)

Description

Inhibition 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.

Publication Title

Up-regulation of endoplasmic reticulum stress-related genes during the early phase of treatment of cultured cortical neurons by the proteasomal inhibitor lactacystin.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE85573
Partially exhausted CD8+ T cells are associated with clinically beneficial response to Teplizumab in new onset type I diabetes
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Treatment, Race

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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