Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Cerebellar Gene Expression Profile Analysis in a Rat Model of Acute Alcohol Intoxication

ABSTRACT: To identify possible target molecules for acute alcohol intoxication therapy, we used microarray analysis to compare cerebella gene expression profiles of control and acute alcohol-intoxicated rats. We first established a model of acute alcohol intoxication in SD rats, and then used rat cDNA microarray to profile mRNA expression in the cerebella of alcohol-intoxicated rats (experimental group) and saline-treated rats (control group). A six chip study using total RNA recovered from three separate experimental groups and three separate control groups. We first established a model of acute alcohol intoxication in SD rats, and then used rat cDNA microarray to profile mRNA expression in the cerebella of alcohol-intoxicated rats (experimental group) and saline-treated rats (control group). Cerebellar tissues from three rats were ground to a mixed sample,so we use 3 rats in one group.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Ji-lai Liu

PROVIDER: E-GEOD-49303 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:T cells undergo autoimmunization following spinal cord injury (SCI) and play both protective and destructive roles during the recovery process. T-cell deficient athymic nude (AN) rats recover better than immunocompetent Sprague-Dawley (SD) rats following spinal cord transection. In the present study, we evaluated locomotor recovery in SD and AN rats following moderate spinal cord contusion. To explain variable locomotor outcome, we assessed whole-genome expression using RNA sequencing, in the acute (1 week post-injury) and chronic (8 weeks post-injury) phases of recovery. AN rats demonstrated greater locomotor function than SD rats only at 1 week post-injury, coinciding with peak T cell infiltration in immunocompetent rats. Genetic markers for T cells and helper T cells were acutely enriched in SD rats, while AN rats expressed genes for Th2 cells, cytotoxic T cells, NK cells, mast cells, IL-1a, and IL-6 at higher levels. Acute enrichment of cell death-related genes suggested that SD rats undergo secondary tissue damage from T cells. Additionally, SD rats exhibited increased acute expression of voltage-gated potassium (Kv) channel-related genes. However, AN rats demonstrated greater chronic expression of cell death-associated genes and less expression of axon-related genes. We put forth a model in which T cells facilitate early tissue damage, demyelination, and Kv channel dysregulation in SD rats following contusion SCI. However, compensatory features of the immune response in AN rats cause delayed tissue death and limit long-term recovery. T cell inhibition combined with other neuroprotective treatment may thus be a promising therapeutic avenue. 2x2 model with 4 groups and 12 total samples. 2 rat strains (athymic nude [AN] and Sprague-Dawley [SD]) and 2 time points (1 week post-injury [acute] and 8 weeks post-injury [chronic]). 3 samples per group, for a total of 12 samples. No technical replicates were performed. Acute SD group = rats 618, 619, and 620. Chronic SD group = rats 605, 606, and 608. Acute AN group = rats 714, 715, and 717. Chronic AN group = rats 707, 712, and 713.

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Cerebellar Gene Expression Profile Analysis in a Rat Model of Acute Alcohol Intoxication

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