Project description:MicroRNAs (miRNAs) are small and endogenously expressed non-coding RNAs that negatively regulate the expression of protein-coding genes at the translational level. Emerging evidence suggests that miRNAs play critical roles in central nervous system under physiological and pathological conditions. However, their expression and functions in status epilepticus (SE) have not been well characterized thus far. Here, we characterized miRNA expression profile in rat hippocampus at 24 hours following SE induced by amygdala stimulation. Hippocampus miRNA profiles of experimental group and control group were generated by deep sequencing, using Hiseq 2000.
Project description:MicroRNAs (miRNAs) are small and endogenously expressed non-coding RNAs that negatively regulate the expression of protein-coding genes at the translational level. Emerging evidence suggests that miRNAs play critical roles in central nervous system under physiological and pathological conditions. However, their expression and functions in status epilepticus (SE) have not been well characterized thus far. Here, we characterized miRNA expression profile in rat hippocampus at 24 hours following SE induced by amygdala stimulation.
Project description:Here, we characterised the effects of experimental status epilepticus on the expression of exosome biosynthesis components and analysed microRNA content in exosome-enriched fractions prepared from the mouse hippocampus. Status epilepticus induced by unilateral intra-amygdala kainic acid resulted in acute subfield-specific, bi-directional changes in transcripts associated with exosome biosynthesis including up-regulation of ESCRT–dependent and –independent pathways. Increased expression of exosome components including Alix were detectable in samples obtained two weeks after status epilepticus and changes occurred in both the ipsilateral and contralateral hippocampus. Small RNAseq analysis of exosome-enriched fractions prepared using two different techniques detected a rich diversity of conserved microRNAs and determined status epilepticus selectively alters microRNA contents, including upregulation of the glia-enriched miR-21a-3p. We also characterized editing sites of the exosome-enriched miRNAs and found six exosome-enriched miRNAs that were Adenosine-to-Inosine (ADAR) edited with the majority of the editing events predicted to occur within miRNA seed regions. However, the prevalence of these editing events was not altered by status epilepticus. These studies demonstrate status epilepticus alters the exosome pathway and its microRNA content, but not editing patterns.
Project description:Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were utilized to prevent many kainate induced status epilepticus changes in gene expression. Total RNA recovered from CA1 of hippocampus of rats receiving scrambled, and saline(controls) or kainate injections (induced status epilepticus)
Project description:Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were used to prevent many kainate induced status epilepticus changes in gene expression. Total RNA recovered from CA1 of hippocampus of rats receiving scrambled or NRSE oligodeoxynucleotides, and kainate injections (induced status epilepticus)
Project description:Epilepsy causes altered gene expression; transient adenosine treatment inhibits progression of epileptogenesis Hippocampus of epileptic rat is hypermethylated compared to naïve; adenosine treatment causes hypomethylation Metylation state in epileptic rats (9 weeks post kainic acid induced status epilepticus) was compared to naïve (untreated) rats and epileptic rats treated with adenosine for 5 days
Project description:Oligodeoxynucleotides used to prevent NRSF binding to NRSE containing genes were utilized to prevent many kainate induced status epilepticus changes in gene expression. Total RNA recovered from CA1 of hippocampus of rats receiving scrambled or NRSE oligodeoxynucleotides, and saline(controls) or kainate injections (induced status epilepticus)
Project description:Transcriptional profiling of mouse ipsilateral hippocampi at 24 hours after intra-amygdala kainic acid-induced status epilepticus followed by either Antagomir-134 or Scramble (control) treatment (intraperitoneal; 30 mg.kg-1)
