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Genome-wide analysis of histone H3K18 lactylation in a kainic acid-induced epilepsy model

ABSTRACT: Metabolic reprogramming has been increasingly linked to epilepsy, but the epigenetic mechanisms connecting altered glucose metabolism to seizure susceptibility remain incompletely understood. In this study, we aimed to investigate whether lactate-associated histone modification contributes to epileptogenesis and to define its downstream transcriptional targets. Using a kainic acid (KA)-induced temporal lobe epilepsy model, we examined genome-wide chromatin occupancy of histone H3 lysine 18 lactylation (H3K18la) in control and epileptic mouse hippocampal tissues by ChIP-seq. The objective of this study was to characterize H3K18la-associated epigenetic changes during epileptogenesis and to identify candidate genes and pathways regulated by this histone mark. These data provide a genome-wide resource for understanding how glycolysis-related histone lactylation is involved in transcriptional regulation during seizure development.

ORGANISM(S): Mus musculus

PROVIDER: GSE326007 | GEO | 2026/07/15

REPOSITORIES: GEO

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Project description:Mesial Temporal Lobe Epilepsy (MTLE) is a chronic disease characterized by recurrent unprovoked partial seizures. Current treatments lack long-term efficacy and typically act only to ameliorate the symptomology, rather than to modify the course of the disease. Chronic kainic acid (KA)-induced models of MTLE mimic prominent histopathological and electroencephalographic features of human MTLE, including hippocampal sclerosis, CA1 neuronal loss, astrogliosis, microgliosis, and electrographic hippocampal discharges. Here we examined the transcriptional profiles of the hippocampus of KA - vs sham-injected mice from epileptogenesis to the stabilization of spontaneous recurring seizures. KA (1 nmol) or saline (sham) was injected unilaterally into the dorsal hippocampus of 12 week old C57BL/6J mice, and the ipsilateral (IL) and contralateral (CL) hippocampi were isolated for whole-genome expression profiling (Illumina microarray) or immunohistochemistry 7, 28 and 60 d later. Differential gene expression analysis of the IL hippocampus indicated that 1349, 484, and 439 genes were significantly (fdr<0.05) altered in KA compared to sham at 7, 28 and 60 d, respectively. 108 genes were altered at all time-points assessed, while others were altered in a time-dependent manner, indicative of distinct hippocampal gene expression profiles across the course of disease. Ingenuity Pathway Analysis revealed that specific immune cell and inflammatory signaling pathways were upregulated at 7 and 28 d, in support of a role of neuroinflammation in the disease etiology. The top canonical pathways profile at 60 d was quite distinct from that at 7 and 28 d, although certain inflammatory pathways were still prevalent, indicative of pathways involved in the maintenance of the disease. Consistent with a role of neuroinflammation in MTLE, immunohistochemical analyses demonstrated time-dependent changes in both the intensity of immunoreactivity and number of Iba1- and GFAP-positive cells. To reveal gene networks not apparent with differential expression data alone, weighted gene co-expression analysis (WGCNA) was performed. A gene network that highly associated with 7 d IL-KA (but not 28 and 60 d) was identified, which may point to changes involved in the process of epileptogenesis. Another gene network revealed a group of genes highly associated with changes occurring at 28 and 60 d, but not 7 d, which may point to molecules involved in the generation of spontaneous recurring seizures. Collectively, results indicate that specific pathways, including many associated with neuroinflammation, are activated in a time-dependent manner in MTLE.

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Genome-wide analysis of histone H3K18 lactylation in a kainic acid-induced epilepsy model

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