Genetic deletion of microRNA-22 blunts the inflammatory transcriptional response to status epilepticus and exacerbates epilepsy in mice

Mice lacking miR-22 displayed normal behavior and brain structure and developed similar status epilepticus after intraamygdala kainic acid compared to wildtype animals. Subsequent continuous EEG monitoring revealed an accelerated and exacerbated epileptogenesis whereby spontaneous seizures began sooner, occurred more frequently and were of longer duration in miR-22-deficient mice. RNA sequencing analysis of the hippocampus of mice during the period of epileptogenesis revealed a widespread suppression of inflammatory signalling in the hippocampus of miR-22-deficient mice. Taken together, these findings indicate a role for miR-22 in establishing early inflammatory responses to status epilepticus. Inflammatory signalling may serve anti-epileptogenic functions and cautions the timing of anti-inflammatory treatments for the treatment of status epilepticus. Overall design: two groups: Wildtype and miR-22-/- mice (n = 4 each) were subjected to status epilepticus. Twenty-four hours later, mice were euthanized and the ipsilateral hippocampus was obtained. Total RNA was extracted and library preparation was performed using an Illumina TruSeq Stranded mRNA Sample Prep Kit (poly-A enrichment)