Global transcriptomic profiling of hypoxic ischemia in an in vivo neonatal mouse model
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE23333 | GEO | 2013/12/31
SECONDARY ACCESSION(S): PRJNA131215
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-12-31 | E-GEOD-23333 | biostudies-arrayexpress
Project description:Hypoxia-ischemia (HI) brain damage is one of the most common causes of neonatal brain injuries, amidst other conditions such as intrauterine infection and perinatal cerebral hemorrhage (Bracci et al., 2006). HI, occurring during the perinatal period, severely affects brain integrity resulting in detrimental long-term neurological morbidity in terms of motor, intellectual, educational and neuropsychological performance deficits (e.g. cerebral palsy, mental retardation, learning disability and epilepsy), and even neonatal mortality (Cowan et al., 2003; Ferriero, 2004; van Handel et al., 2007; Shalak and Perlman, 2004). Current therapeutic interventions fail to provide substantial reversal of HI brain injuries and improvement in overall cognitive function. Recent clinical studies demonstrated that post-HI hypothermia provide moderate neuroprotection but fail to show any significant reduction in neonatal morbidity and mortality (Shankaran et al., 2005). We would like to investigate the transcriptional effects of HI on neonatal brain, and if hypoxic pre-conditioning is beneficial to the reduction of brain damage.
2013-12-31 | GSE23319 | GEO
Project description:Hypoxia-ischemia (HI) brain damage is one of the most common causes of neonatal brain injuries, amidst other conditions such as intrauterine infection and perinatal cerebral hemorrhage (Bracci et al., 2006). HI, occurring during the perinatal period, severely affects brain integrity resulting in detrimental long-term neurological morbidity in terms of motor, intellectual, educational and neuropsychological performance deficits (e.g. cerebral palsy, mental retardation, learning disability and epilepsy), and even neonatal mortality (Cowan et al., 2003; Ferriero, 2004; van Handel et al., 2007; Shalak and Perlman, 2004). Current therapeutic interventions fail to provide substantial reversal of HI brain injuries and improvement in overall cognitive function. Recent clinical studies demonstrated that post-HI hypothermia provide moderate neuroprotection but fail to show any significant reduction in neonatal morbidity and mortality (Shankaran et al., 2005). We would like to investigate the transcriptional effects of HI on neonatal brain, and if hypoxic pre-conditioning is beneficial to the reduction of brain damage.
2013-12-31 | GSE23317 | GEO
Project description:Hypoxia-ischemia (HI) brain damage is one of the most common causes of neonatal brain injuries, amidst other conditions such as intrauterine infection and perinatal cerebral hemorrhage (Bracci et al., 2006). HI, occurring during the perinatal period, severely affects brain integrity resulting in detrimental long-term neurological morbidity in terms of motor, intellectual, educational and neuropsychological performance deficits (e.g. cerebral palsy, mental retardation, learning disability and epilepsy), and even neonatal mortality (Cowan et al., 2003; Ferriero, 2004; van Handel et al., 2007; Shalak and Perlman, 2004). Current therapeutic interventions fail to provide substantial reversal of HI brain injuries and improvement in overall cognitive function. Recent clinical studies demonstrated that post-HI hypothermia provide moderate neuroprotection but fail to show any significant reduction in neonatal morbidity and mortality (Shankaran et al., 2005). We would like to investigate the transcriptional effects of HI on neonatal brain, and if hypoxic pre-conditioning is beneficial to the reduction of brain damage. Microarray analysis was performed on the cortex of neonatal brains using Illumina mouse Ref8 V2 genechips. The right common carotid artery was exposed through a ventral midline neck incision and permanently occluded by electrocoagulation, The wound was sutured and mouse pups were returned to their mother for 1.5M-bM-^@M-^S2 h. Sham control and pre-conditioned mice (n = 4) underwent the identical procedure, without carotid artery occlusion. Pups were then placed in an 8% O2/92% N2 humidified chamber at 37M-BM-0C for 1 h with tissue extraction taking place 3h, 8h and 24h thereafter (n=4 respectively). Sham controls were included in this study too (n=4 respectively).
2013-12-31 | E-GEOD-23317 | biostudies-arrayexpress
Project description:Hypoxia-ischemia (HI) brain damage is one of the most common causes of neonatal brain injuries, amidst other conditions such as intrauterine infection and perinatal cerebral hemorrhage (Bracci et al., 2006). HI, occurring during the perinatal period, severely affects brain integrity resulting in detrimental long-term neurological morbidity in terms of motor, intellectual, educational and neuropsychological performance deficits (e.g. cerebral palsy, mental retardation, learning disability and epilepsy), and even neonatal mortality (Cowan et al., 2003; Ferriero, 2004; van Handel et al., 2007; Shalak and Perlman, 2004). Current therapeutic interventions fail to provide substantial reversal of HI brain injuries and improvement in overall cognitive function. Recent clinical studies demonstrated that post-HI hypothermia provide moderate neuroprotection but fail to show any significant reduction in neonatal morbidity and mortality (Shankaran et al., 2005). We would like to investigate the transcriptional effects of HI on neonatal brain, and if hypoxic pre-conditioning is beneficial to the reduction of brain damage. Microarray analysis was performed on the striatum of neonatal brains using Illumina mouse Ref8 V2 genechips. The right common carotid artery was exposed through a ventral midline neck incision and permanently occluded by electrocoagulation, The wound was sutured and mouse pups were returned to their mother for 1.5M-bM-^@M-^S2 h. Sham control and pre-conditioned mice (n = 4) underwent the identical procedure, without carotid artery occlusion. Pups were then placed in an 8% O2/92% N2 humidified chamber at 37M-BM-0C for 1 h with tissue extraction taking place 3h, 8h and 24h thereafter (n=4 respectively). Sham controls were included in this study too (n=4 respectively).
2013-12-31 | E-GEOD-23319 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2011-01-10 | GSE23163 | GEO
Project 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.
2013-12-31 | GSE23651 | GEO
Project 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. Microarray analysis was performed on Illumina Rat Ref12V1 beadchips. Right cortex RNA samples were collected at two time-points (8h and 24h ) respectively for all three experimental conditions: Sham (n=4), vehicle (i.e. ischemic injury with i.c.v. injection 80% DMSO; n=4) and treatment (injury plusi.c.v.injection of 30mM ZM447439 in 80% DMSO; n=4).
2013-12-31 | E-GEOD-23651 | biostudies-arrayexpress
Project 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-ventricularly 30min post-ischemia induction to determine its efficacy in reduction of neuronal damage in terms of infarct volume.
2013-12-31 | GSE25556 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-12-31 | E-GEOD-25676 | biostudies-arrayexpress