MicroRNA-219 alleviates glutamate-induced neurotoxicity in cultured hippocampal neurons by targeting calmodulin-dependent protein kinase II gamma.

ABSTRACT: Septic encephalopathy is a frequent complication of sepsis, but there are few studies examining the role of microRNAs (miRs) in its pathogenesis. In this study, a miR-219 mimic was transfected into rat hippocampal neurons to model miR-219 overexpression. A protective effect of miR-219 was observed for glutamate-induced neurotoxicity of rat hippocampal neurons, and an underlying mechanism involving calmodulin-dependent protein kinase II γ (CaMKIIγ) was demonstrated. miR-219 and CaMKIIγ mRNA expression induced by glutamate in hippocampal neurons was determined by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). After neurons were transfected with miR-219 mimic, effects on cell viability and apoptosis were measured by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenylte

SUBMITTER: Wang T 

PROVIDER: S-EPMC6065221 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature