Long non-coding RNA H19 contributes to apoptosis of hippocampal neurons by inhibiting let-7b in a rat model of temporal lobe epilepsy

• Published in: Cell death & disease Vol. 9; no. 6; pp. 617 - 13
• Main Authors: Han, Chun-Lei, Ge, Ming, Liu, Yun-Peng, Zhao, Xue-Min, Wang, Kai-Liang, Chen, Ning, Hu, Wei, Zhang, Jian-Guo, Li, Liang, Meng, Fan-Gang
• Format: Journal Article
• Language: English
• Published: England Springer Nature B.V 23.05.2018; Nature Publishing Group UK
• Subjects: Apoptosis; Brain injury; Epilepsy; Hippocampus; Latent period; miRNA; Non-coding RNA; Post-transcription; Rodents; Sclerosis; Seizures; Temporal lobe
• ISSN: 2041-4889; 2041-4889
• DOI: 10.1038/s41419-018-0496-y

Temporal lobe epilepsy (TLE) is one of the most common types of intractable epilepsy, characterized by hippocampal neuron damage and hippocampal sclerosis. Long noncoding RNAs (lncRNAs) have been increasingly recognized as posttranscriptional regulators. However, their expression levels and functions in TLE remain largely unknown. In the present study, TLE rat model is used to explore the expression profiles of lncRNAs in the hippocampus of epileptic rats using microarray analysis. Our results demonstrate that H19 is the most pronouncedly differentiated lncRNA, significantly upregulated in the latent period of TLE. Moreover, the in vivo studies using gain- and loss-of-function approaches reveal that the overexpression of H19 aggravates SE-induced neuron apoptosis in the hippocampus, while inhibition of H19 protects the rats from SE-induced cellular injury. Finally, we show that H19 might function as a competing endogenous RNA to sponge microRNA let-7b in the regulation of cellular apoptosis. Overall, our study reveals a novel lncRNA H19-mediated mechanism in seizure-induced neural damage and provides a new target in developing lncRNA-based strategies to reduce seizure-induced brain injury.