GSE191038
Transcriptome results in hippocampus and cortex of KCNMA1-/- (BK KO) mice.
In this study, we used RNA-Seq to analyze the transcriptome of BK KO/WT mice hippocampus and cortex, and performed transcriptome profiling to characterize the differentially expressed genes. A total of 652 genes were screened with the threshold of significance at P < 0.05 and |log2foldchange| > 0.58, among which 382 genes were down-regulated and 270 genes were up-regulated in hippocampus tissues. In cortex tissues, we detected a total of 561 differentially expressed genes with the threshold of significance at P < 0.05 and |log2foldchange| > 0.58, including 162 up-regulated genes and 399 down-regulated genes. In order to better understand the potential functions of differentially expressed genes, Gene Ontology (GO) enrichment analysis was carried out to assess the involved pathways. Biological process pathway in GO analysis results showed that development process and biological adhesion were enriched. The results of kyoto encyclopedia of genes and genomes (KEGG) showed that insulin secretion, axon guidance, p53 signaling pathway, HIF-1 signaling pathway and calcium signaling pathway were enriched in hippocampus. On the other hand, cortical KEGG results showed that cell adhesion molecules (CAMs), ECM-receptor interaction, phagosome and calcium signaling pathway were enriched. Dysregulation of gene expression, especially astrocyte activation, neuroinflammation and autophagy, might be the molecular mechanism of BK-LOF meditated epilepsy. This study explores the possible mechanism of epilepsy by transcriptome, reveals the relationship between KCNMA1-LOF and epilepsy, and provides a possible molecular template for individualized treatment of epilepsy. Overall design: Hippocampus and cortex mRNA profiles of  WT and BK KO mice.