Correlation between IL-10 and microRNA-187 expression in epileptic rat hippocampus and patients with temporal lobe epilepsy

Accumulating evidence is emerging that microRNAs (miRs) are key regulators controlling neuroinflammatory processes, which are known to play a potential role in the pathogenesis of temporal lobe epilepsy (TLE). The aim of the present study was to investigate the dynamic expression pattern of interleu...

Full description

Bibliographic Details
Main Authors: Walid A. Alsharafi, Bo eXiao, Mutasem M Abuhamed, Fangfang eBi, Zhaohui eLuo
Format: Article
Language:English
Published: Frontiers Media S.A. 2015-12-01
Series:Frontiers in Cellular Neuroscience
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00466/full
Description
Summary:Accumulating evidence is emerging that microRNAs (miRs) are key regulators controlling neuroinflammatory processes, which are known to play a potential role in the pathogenesis of temporal lobe epilepsy (TLE). The aim of the present study was to investigate the dynamic expression pattern of interleukin (IL)–10 as an anti-inflammatory cytokine and miR-187 and post-transcriptional inflammation-related miRNA in the hippocampus of a rat model of status epilepticus (SE) and patients with TLE. We performed a real-time quantitative PCR and western blot on rat hippocampus (2 hours, 7 days, 21 days and 60 days) following pilocarpine-induced SE, and on hippocampus obtained from TLE patients and normal controls. To detect the relationship between IL-10 and miR-187 on neurons, lipopolysaccharide (LPS) and IL-10-stimulated neurons were prepared. Furthermore, we identified the effect of antagonizing of miR-187 by its antagomir on IL-10 secretion. Here we reported that that IL-10 secretion and miR-187 expression levels are inversely correlated after SE.. In patients with TLE, the expression levels of IL-10 was also significantly upregulated, whereas miR-187 expression was significantly downregulated. Moreover, miR-187 expression was significantly reduced following IL-10 stimulation in an IL-10–dependent manner. On the other hand, antagonizing miR-187 reduced the production of IL-10 in hippocampal tissues of rat model of SE. Our findings demonstrate a critical role of miR-187 in the physiological regulation of IL-10 anti-inflammatory responses and elucidate the role of neuro-inflammation in the pathogenesis of TLE. Therefore, modulation of the IL-10 / miR-187 axis may be a new therapeutic approach for TLE.
ISSN:1662-5102