Differential DNA Methylation Profiles in Patients with Temporal Lobe Epilepsy and Hippocampal Sclerosis ILAE Type I

• DOI: 10.1007/s12031-020-01780-9
• Publication Date: 2021-01-05T17:22:14Z
• Authors: Wang Zhang; Haiyang Wang; Binchao Liu; Miaomiao Jiang; Yifei Gu; Shi Yan; Xian Han; Alicia Y. Hou; Chongyang Tang; Zhenfeng Jiang; Hong Shen; Meng Na; Zhiguo Lin
• Keywords: Adult; Male; 0301 basic medicine; Sclerosis; Adolescent; Chromosomal Proteins, Non-Histone; Membrane Proteins; DNA Methylation; Hippocampus; Repressor Proteins; Epigenome; 03 medical and health sciences; Epilepsy, Temporal Lobe; ras GTPase-Activating Proteins; Humans; Female

Hippocampal sclerosis (HS) is one of the most prevalent pathological types of temporal lobe epilepsy (TLE), and it significantly affects patient prognoses. The methylation of DNA plays an important role in the development of epilepsy. However, few studies have focused on HS subtypes to determine DNA methylation profiles in TLE. This study aimed to determine the pathogenesis of TLE from an epigenetic perspective in patients with TLE-HS type I (TLE-HSTI) and TLE without HS (TLE-nHS) using whole-genome bisulfite sequencing (WGBS). We defined 1171 hypermethylated and 2537 hypomethylated regions and found 632 differentially methylated genes (DMG) in the promoter region that were primarily involved in the regulation of various aspects of epilepsy development. Twelve DMG overlapped with differentially expressed genes (DEG) in the promoter region, and RT-qPCR findings revealed significant overexpression of the SBNO2, CBX3, RASAL3, and TMBIM4 genes in TLE-HSTI. We present the first systematic analysis of methylation profiles of TLE-HSTI and TLE-nHS from an epigenetic perspective using WGBS. Overall, our preliminary data highlight the underlying mechanism of TLE-HSTI, providing a new perspective for guiding treatment of TLE.