Abnormal Weakening of DNA Methylation around the Gene Promoter in Temporal Lobe Epilepsy.

BACKGROUND

The solute carrier (SLC) superfamily, which transports solutes across biological membranes, includes four members (SLC2A1, SLC6A1, SLC9A64, and SLC35A2) that have been linked to epilepsy. This study sought to examine the DNA methylation patterns near the promoters of these genes in temporal lobe epilepsy (TLE), as DNA methylation is a crucial epigenetic modification that can impact gene expression.

METHODS

The study comprised 38 individuals with TLE and 38 healthy controls. Methylation experiments were performed using peripheral blood, while demethylation experiments were carried out using SH-SY5Y cells with the DNA methylation inhibitor decitabine.

RESULTS

A significant difference was observed in the DNA methylation rate of between TLE patients and controls, with TLE patients showing a lower rate (4.81% vs. 5.77%, = 0.0000), which remained significant even after Bonferroni correction ( = 0.0000). Based on the hypomethylated in TLE, a predictive model was established that showed promise in distinguishing and calibrating TLE. In the TLE group, there were differences in DNA methylation rates of between the young patients and the older controls (4.42% vs. 5.22%, = 0.0004). A similar trend ( = 0.0436) was noted after adjusting for sex, age at onset, and drug response. In addition, the study found that DNA methylation had a silencing impact on the expression of the gene in SH-SY5Y cells, which were treated with decitabine at a set dose gradient.

CONCLUSIONS

The evidence suggests that lower methylation of may stimulate transcription in TLE, however, further investigation is necessary to confirm the exact mechanism.

© 2024 The Author(s). Published by IMR Press.