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Editorial
. 2017 Jul 11;8(28):45040-45041.
doi: 10.18632/oncotarget.18364.

Epigenetic control of epileptogenesis by miR-146a

Valentina Iori  1 , Eleonora Aronica  1 , Annamaria Vezzani  1
Affiliations
Editorial

Epigenetic control of epileptogenesis by miR-146a

Valentina Iori et al. Oncotarget. .
No abstract available

Keywords: disease-modification; epilepsy; microRNA; neuroinflammation; seizures.

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Figures

Figure 1
Figure 1. IL-1R1/TLR4 signaling inhibition by miR-146a mimic in neurons and astrocytes
The activation of IL-1R1/TLR4 axis promotes seizure generation in susceptible brain areas by a twofold mechanism mediated by IL-1β and HMGB1 activation of neuronal or astrocyte receptors. A. Activation of IL-1R1/TLR4 axis in neurons provokes hyper-excitability by enhancing Ca2+ influx via the glutamate-sensitive N-methyl-D-aspartate receptor (NMDAR). This fast-onset posttranslational response involves ceramide-induced Src kinase phosphorylation (P) of the NR2B subunit of the NMDAR which regulates Ca2+ influx [5]. B. Activation of IL-1R1/TLR4 axis in astrocytes induces NF-κB- and AP-1 dependent transcription of inflammatory genes. miR-146a mimic (red cross) down-regulates IRAK1/2 and TRAF6 intracellular proteins (downward arrow) which are required for IL-1R1/TLR4 signal transduction. IL-1R1/TLR4 axis inhibition by miR-146a mimic -or using a combination of drugs, namely VX-765 that blocks IL-1β biosynthesis, and Cyanobacterial LPS, a TLR4 antagonist [6]- reduces hyper-excitability and neuroinflammation (downward arrow) in mice developing epilepsy, thus resulting in therapeutic outcomes.
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