Abstract
BackgroundTo investigate the effect of long-term febrile convulsions on gene expression in mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) and explore the molecular mechanism of MTLE-HS.MethodsMicroarray data of MTLE-HS were obtained from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) between MTLE-HS with and without febrile seizure history were screened by the GEO2R software. Pathway enrichment and gene ontology of the DEGs were analyzed using the DAVID online database and FunRich software. Protein–protein interaction (PPI) networks among DEGs were constructed using the STRING database and analyzed by Cytoscape.ResultsA total of 515 DEGs were identified in MTLE-HS samples with a febrile seizure history compared to MTLE-HS samples without febrile seizure, including 25 down-regulated and 490 up-regulated genes. These DEGs were expressed mostly in plasma membrane and synaptic vesicles. The major molecular functions of those genes were voltage-gated ion channel activity, extracellular ligand-gated ion channel activity and calcium ion binding. The DEGs were mainly involved in biological pathways of cell communication signal transduction and transport. Five genes (SNAP25, SLC32A1, SYN1, GRIN1, and GRIA1) were significantly expressed in the MTLE-HS with prolonged febrile seizures.ConclusionThe pathogenesis of MTLE-HS involves multiple genes, and prolonged febrile seizures could cause differential expression of genes. Thus, investigations of those genes may provide a new perspective into the mechanism of MTLE-HS.
Highlights
To investigate the effect of long-term febrile convulsions on gene expression in mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) and explore the molecular mechanism of MTLE-HS
Identification of Differentially expressed genes (DEGs) in MTLE-HS Using criteria of |log FC| > 1 and adjusted P value < 0.05, 515 DEGs from the GSE28674 dataset were identified between samples of MTLE-HS with and without febrile seizure history, containing 25 down-regulated and 490 up-regulated genes in MTLE-HS with prolonged febrile seizure (Fig. 1, Additional file 1)
Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and gene ontology (GO) enrichment analyses of DEGs GO cell component (CC) analysis revealed that the DEGs were mainly enriched in plasma membrane and synaptic vesicle and axon (Fig. 2a); GO molecular function (MF) analysis revealed that the DEGs were significantly enriched in voltage-gated ion channel activity, calcium ion binding and extracellular ligand-gated ion channel activity (Fig. 2b)
Summary
To investigate the effect of long-term febrile convulsions on gene expression in mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) and explore the molecular mechanism of MTLE-HS. Epilepsy is characterized by sudden attacks and recurrent seizures due to abnormal excessive neuronal discharges [1] It can occur at any age and currently has affected about 70 million people worldwide [2]. Temporal lobe epilepsy is a focal type of epilepsy characterized by recurrent lesions in the temporal lobe, most commonly occurring in the medial lobe. It is related with a variety of mental phenomena, including hallucinations, cognitive impairment and emotional experience. Mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) is one of the common epilepsy syndromes worldwide, which commonly arises from longduration seizures, especially febrile status epilepticus, in the early life [3, 4]. Current evidence suggests that MTLEHS is closely related to febrile convulsion, with its pathogenesis involving epigenetic regulation and genetic susceptibility
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