MAPK/ERK activation determines a distinct transcriptional program following neuronal activity in the murine hippocampus
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE88723 | GEO | 2017/06/14
SECONDARY ACCESSION(S): PRJNA348353
REPOSITORIES: GEO
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Project description:This study aims to investigate age-specific, time-dependent changes in gene expression that may underlie the priming effect of early-life seizures by looking at the sequence of gene expression patterns in the hippocampus at various times following Kainate induced seizures at postnatal day (P) 15. Keywords: other
2004-03-29 | GSE1156 | GEO
Project description:This SuperSeries is composed of the following subset Series:; GSE1831: Temporal analysis of P15 hippocampus in kainate-induced seizures. Koh-2K08NS002068-04; GSE1834: Temporal analysis of hippocampus in kainate-induced seizures. Koh-7K08NS002068-05-3 Experiment Overall Design: Refer to individual Series
2007-10-10 | E-GEOD-4236 | biostudies-arrayexpress
Project description:Kanate was used to induce seizures in mice, and gene expression in the hippocampus was measured
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Project description:EZH2 is a key epigenetic regulator that catalyzes histone methylation to effect transcriptional repression. Preliminary data suggested that EZH2 induction is a protective response mounted by the brain in response to seizures. To investigate the impact of EZH2 deletion in hippocampal neurons under pathological conditions, we generated whole transcriptome profiles using RNA sequencing in saline and kainate-treated wild-type (EZH2nWT) mice, as well as homozygous EZH2 neuronal knockout (EZH2nHom) mice. Our results reveal significant alterations in gene expression patterns in the hippocampus of EZH2nHom compared to EZH2nWT mice, particularly following kainate-induced seizures. Overall, our study provides valuable insights into the transcriptional changes induced by EZH2 deletion in hippocampal neurons, highlighting its importance in regulating gene expression in response to epileptogenic insults.
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Project description:The mammalian genome contains two ERK/MAP kinase kinase genes, Mek1 and Mek2, which encode dual-specificity kinases responsible for ERK/MAP kinase activation. To define the function of ERK/MAPK signaling pathway in lung development, we performed tissue-specific deletions of Mek1 function in a Mek2 null background. Inactivation of both Mek genes in mesenchyme resulted in several phenotypes including giant omphalocele, skeletal defects, pulmonary hypoplasia, abnormal trachea patterning, and death at birth. Microarray analysis with RNA extracted from lungs of E15.5 Dermo1+/Cre, Mek1+/flox;Mek2-/-;Dermo1+/Cre and Mek1flox/flox;Mek2-/-;Dermo1+/Cre embryos was performed to evaluate the molecular impact of the loss of all Mek alleles in mesenchyme on lung development. . Total RNA was isolated from lungs of E15.5 Dermo1+/Cre embryos (control), from E15.5 Mek1+/flox;Mek2- /-;Dermo1+/Cre embryos (experimental) and from E15.5 Mek1flox/flox;Mek2-/-;Dermo1+/Cre embryos (experimental). Four specimens were analyzed per genotype.
2014-09-02 | E-GEOD-51643 | biostudies-arrayexpress
Project description:Mesial temporal lobe epilepsy (MTLE) is the most common medically refractory epilepsy syndrome; kainic acid (KA) induced seizures have been studied as a MTLE model as limbic seizures produced by systemic injections of KA result in a distinctive pattern of neurodegeneration in the hippocampus that resembles human hippocampal sclerosis. In our "2-hit" seizure model, animals subjected to seizures during week 2 of life become more susceptible to seizures later in life and sustain extensive hippocampal neuronal injury after second KA seizures in adulthood. Using high-density oligonucleotide gene arrays, we began to elucidate the molecular basis of this priming effect of early-life seizures and of the age-specific neuroprotection against seizure-induced neuronal injury. We seek to identify target genes for epileptogenesis and cell death by selecting transcripts that are differentially regulated at various times in the P15 and P30 hippocampus. To screen for and identify candidate genes responsible for epileptogenesis and seizure-induced cell death. We hypothesize that active process of cell death signaling and long-term synaptic changes leading to chronic epilepsy is mediated by distinct transcriptional responses in mature brain that are different from those in immature brain. We will select for transcripts that are highly regulated at 1, 6, 24, 72 and 240 hours (h) after KA-induced seizures at P30 compared to P15. These differentially regulated genes will serve as potential target genes for therapeutic intervention. Highly regulated genes identified in our array analysis will then be confirmed by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Causative roles of select genes will be directly tested by gene silencing using RNA interference technology or by gene delivery using viral vectors.
2008-06-11 | E-GEOD-1834 | biostudies-arrayexpress
Project description:Thiele2013 - Hippocampus neuronal cells
The model of hippocampus neuronal cells metabolism is derived from the community-driven global reconstruction of human metabolism (version 2.02, MODEL1109130000
).
This model is described in the article:
A community-driven global reconstruction of human metabolism.
Thiele I, et al
.
Nature Biotechnology
Abstract:
Multiple models of human metabolism have been reconstructed, but each represents only a subset of our knowledge. Here we describe Recon 2, a community-driven,
consensus 'metabolic reconstruction', which is the most comprehensive representation of human metabolism that is applicable to computational modeling. Compared
with its predecessors, the reconstruction has improved topological and functional features, including ~2x more reactions and ~1.7x more unique metabolites. Using
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data and drug information onto Recon 2 demonstrates its potential for integrating and analyzing diverse data types. Using protein expression data, we automatically
generated a compendium of 65 cell type-specific models, providing a basis for manual curation or investigation of cell-specific metabolic properties. Recon 2 will
facilitate many future biomedical studies and is freely available at http://humanmetabolism.org/.
This model is hosted on BioModels Database
and identified by: MODEL1310110034
.
To cite BioModels Database, please use: BioModels Database: An enhanced,
curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer
to CC0 Public Domain Dedication
for more information.
2005-01-01 | MODEL1310110034 | BioModels
Project description:Serial analysis of gene expression (SAGE) was used to get a global view of the gene profile in human hippocampus. A library were generated from control hippocampus, obtained by rapid autopsy. Keywords: hippocampus human inventory genes Control hippocampus (used to construct the SAGE control library) was obtained from a 48 years old man without history of seizures or other neurological diseases and no brain abnormalities at autopsy and histologically normal hippocampus. Autopsy was performed within 4 hours after death. Tissue was snap-frozen and stored at –80 0C until use. Total RNA was isolated from control hippocampus and hippocampal surgical specimens, using the Trizol method according to the manufacturer’s instructions (Invitrogen - Life Technologies, The Netherlands). Part of the anterior hippocampus of control (including sectors CA1- CA4 and dentate gyrus, DG) was used. Poly(A)+ RNA isolation, cDNA synthesis and all subsequent steps of the SAGE procedure were essentially performed as described (Velculescu et al., 1995) with minor modifications given previously (Michiels et al., 1999).
2005-12-29 | E-GEOD-3928 | biostudies-arrayexpress
Project description:Early childhood convulsions have been correlated with hippocampal neuron loss in patients with intractable temporal lobe epilepsy. Using a "two-hit" rat seizure model, we have shown that animals subjected to kainate (KA)- or hypoxia-induced seizures during early postnatal period showed no cell death, yet sustained more extensive neuronal death after second seizures in adulthood. An early life seizure, without causing overt cellular injury, predisposes the brain to the damaging effect of seizures in later life. Cellular and molecular changes that accompany early seizures and that lead to subsequent epileptogenesis and increased susceptibility to seizure-induced neuronal injury, however, remain poorly understood. We propose to investigate age-specific, time-dependent changes in gene expression that may underlie this priming effect of early-life seizures. We will determine the sequence of gene expression pattern in the hippocampus at various times following KA induced seizures at postnatal day (P) 15. Previous studies have shown that AMPA receptor subtype of glutamate receptors play a crucial role in the age-specific vulnerability and in the long-term epileptogenic effects of perinatal hypoxia seizures. We found that AMPA receptor antagonists block the increased susceptibility caused by early life seizures to later seizures and seizure-induced brain damage. We hypothesize that an alteration of AMPA receptor composition is one of many changes caused by early-life seizures that leads to an increase in Ca2+ permeability, which then results in cascade of downstream events and modifies array of gene expression that promote epileptogenesis and susceptibility to neuronal death in later life. We will examine three time points: 1hr, 72 hr, and 15 days following systemic KA-induced seizures at P15 as we have previously observed structural changes within the hippocampus at these time points. Within an hour of KA seizures, a marked swelling of dendrites, disassembly of dendritic microtubules and glycogen depletion are observed by electron microscopy. Within 5 days, basal dendrites of CA3 hippocampal pyramidal neurons show abnormal spine morphology and decreased branching pattern. 15 days after the seizures, aberrant growth of mossy fibers in the CA3 stratum oriens is observed in animals exposed to KA. Ten hippocampi will be pooled from five animals treated with KA (3mg/kg i.p.) and from five littermate controls injected with PBS. Animals will be decapitated and hippocampi will be rapidly dissected from the brain, flash frozen in liquid nitrogen, and stored at -80C until extraction of total RNA, which will be sent to the center. We will provide 4 tissue samples-2 controls and 2 KA, each a pool of five animals - for each time points. Mixing tissues from multiple rats will normalize single nucleotide polymorphisms and tissue heterogeneity.
2008-06-11 | E-GEOD-1831 | biostudies-arrayexpress
Project description:The mammalian genome contains two ERK/MAP kinase kinase genes, Mek1 and Mek2, which encode dual-specificity kinases responsible for ERK/MAP kinase activation. To define the function of ERK/MAPK signaling pathway in lung development, we performed tissue-specific deletions of Mek1 function in a Mek2 null background. Inactivation of both Mek genes in mesenchyme resulted in several phenotypes including giant omphalocele, skeletal defects, pulmonary hypoplasia, abnormal trachea patterning, and death at birth. Microarray analysis with RNA extracted from lungs of E15.5 Dermo1+/Cre, Mek1+/flox;Mek2-/-;Dermo1+/Cre and Mek1flox/flox;Mek2-/-;Dermo1+/Cre embryos was performed to evaluate the molecular impact of the loss of all Mek alleles in mesenchyme on lung development. .
2014-09-02 | GSE51643 | GEO