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Lipid signaling during neuronal degeneration in KA-treated mice

ABSTRACT: Lipid homeostasis is dysregulated in several forms of neurodegeneration. Here we examined changes in sterols, neutral lipids and transcripts that control their homeostasis during the neuronal death induced in the CA1 region of mouse hippocampus by focal kainic acid (KA) injection. We defined changes in the lipid economy of neurons and glial cells by staining for neutral lipids and for free cholesterol. Lipid droplets filled with neutral lipids were induced in microglia at ~24 hrs after KA-treatment. At 2-4 days after injection, filipin staining revealed punctate deposits of free cholesterol in neuronal somata. These changes were correlated with alterations in cellular organelles observed in electron microscopy and transcriptomic changes obtained with RNA-seq of tissue from the CA1 region. Mitochondria, the innate inflammatory response and lipids. Lipid droplet transcriptome. Cholesterol economy. Lipids and phagocytosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE99577 | GEO | 2019/09/23

REPOSITORIES: GEO

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Project description:In this study we used microarray analysis to reveal the gene expression profile of the hippocampal CA1 subregion, which was laser-capture microdissected one week after kainic acid (KA)-induced status epilepticus (SE) in postnatal day 21 (P21) rats. These rats are developmentally roughly comparable to juvenile children, and KA-induced SE leads to selective damage of hippocampal CA1 pyramidal neurons in this age group while saving neurons of the other sub-regions. We searched for alterations in the gene expression pattern during the early epileptogenetic phase, i.e. one week after SE, and compared the results with those of age-matched control rats. To detect specifically changes in the CA1 pyramidal neurons, we used the laser-capture microdissection technique that allows the precise isolation of the region of interest. The RNA of this region was isolated, amplified, and labeled, and then hybridized to Illumina RatRef-12 Expression BeadChip Arrays. The gene expression data generated from the microarray was first normalized by the guantile normalization method, and then filtered by using the empirical Bayes method, and the contrasts were created by using the Limma R/Bioconductor. Finally, the data was clustered by using the non-hierarchical K-means clustering for genes, and the pathway analysis was performed by âGene set testâ, which analyzes the statistical significance of a set of genes simultaneously ranked by p-value and generates the KEGG categories (Chipster manual). The Illumina microarray analysis with the Chipster software v1.1.0 (http://chipster.csc.fi; CSC, Espoo, Finland) generated a total of 1592 differently expressed genes in the CA1 subregion of KA-treated rats compared to control rats. Using the K-means method the genes were classified in 10 different clusters. The subsequent KEGG-test for the probe set over-representation analysis revealed the 15 significantly (p<0.05) changed KEGG-pathways in response to KA-treatment, e.g. oxidative phosphorylation (26 genes changed), and long-term potentiation (LTP; 18 genes changed). Some of the differentially expressed genes were also identified to be involved in Ca2+ homeostasis, gliosis, inflammation, and GABAergic transmission.

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Lipid signaling during neuronal degeneration in KA-treated mice

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