• Users Online: 2378
  • Home
  • Print this page
  • Email this page
Year : 2018  |  Volume : 13  |  Issue : 7  |  Page : 1216-1224

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

1 Department of Emergency, First Affiliated Hospital of Soochow University, Suzhou; Department of Emergency, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China
2 Department of Pediatrics, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China
3 Medical College of Nantong University, Nantong, Jiangsu Province, China
4 Department of Emergency, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China

Correspondence Address:
Feng Xu
Department of Emergency, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province
Login to access the Email id

Source of Support: This study was supported by the National Natural Science Foundation of China, No. 81101159; the Natural Science Foundation of Jiangsu Province of China, No. BK20151268, Conflict of Interest: None

DOI: 10.4103/1673-5374.235059

Rights and Permissions

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-diphenyltetrazolium bromide (MTT) assay and flow cytometry. In addition, a luciferase reporter gene system was used to confirm CaMKIIγ as a target gene of miR-219. Western blot assay and rescue experiments were also utilized to detect CaMKIIγ expression and further verify that miR-219 in hippocampal neurons exerted its effect through regulation of CaMKIIγ. MTT assay and qRT-PCR results revealed obvious decreases in cell viability and miR-219 expression after glutamate stimulation, while CaMKIIγ mRNA expression was increased. MTT, flow cytometry, and caspase-3 activity assays showed that miR-219 overexpression could elevate glutamate-induced cell viability, and reduce cell apoptosis and caspase-3 activity. Moreover, luciferase CaMKIIγ-reporter activity was remarkably decreased by co-transfection with miR-219 mimic, and the results of a rescue experiment showed that CaMKIIγ overexpression could reverse the biological effects of miR-219. Collectively, these findings verify that miR-219 expression was decreased in glutamate-induced neurons, CaMKIIγ was a target gene of miR-219, and miR-219 alleviated glutamate-induced neuronal excitotoxicity by negatively controlling CaMKIIγ expression.

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded245    
    Comments [Add]    
    Cited by others 8    

Recommend this journal