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Optimized Management of Endovascular Treatment for Acute Ischemic Stroke
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LncRNA-1810034E14Rik reduces microglia activation in experimental ischemic stroke

Xi Zhang1,2, Xiao-Lei Zhu1,2, Bi-Ying Ji1,2

  • 1Department of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, 210008, China.

Journal of Neuroinflammation
|April 10, 2019
PubMed
Abstract

Insights

LncRNA-1810034E14Rik is decreased in ischemic stroke models. Overexpressing this long non-coding RNA reduces brain damage and inflammation, suggesting it as a therapeutic target.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Microglial cell activation is crucial in neuroinflammation following ischemic stroke.
  • Inhibiting microglial activation presents a potential therapeutic strategy for stroke treatment.

Purpose of the Study:

  • To investigate the role of long non-coding RNAs (lncRNAs) in microglial cell inflammation during ischemic stroke.
  • To determine the therapeutic potential of LncRNA-1810034E14Rik in ischemic stroke models.

Main Methods:

  • Established in vitro (oxygen-glucose deprivation) and in vivo (MCAO mouse model) ischemic stroke models.
  • Utilized microarray, RT-qPCR, ELISA, immunofluorescence, and Western blotting to analyze lncRNA and inflammatory marker expression and microglial activation.

Main Results:

  • LncRNA-1810034E14Rik expression was significantly reduced in ischemic conditions.
  • Overexpression of LncRNA-1810034E14Rik decreased infarct volume and brain damage in MCAO mice.
  • LncRNA-1810034E14Rik suppressed microglial activation, inflammatory cytokine production, and p65 phosphorylation.

Conclusions:

  • LncRNA-1810034E14Rik exhibits an anti-inflammatory role in ischemic stroke.
  • This lncRNA regulates p65 phosphorylation, indicating its potential as a therapeutic target for stroke treatment.
Keywords:
Ischemic strokeMicroglial cellslncRNA-1810034E14Rikp65

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