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miRNA-3473b contributes to neuroinflammation following cerebral ischemia

Xiaoyu Wang1,2,3, Shuangshuang Chen1,2, Jingshu Ni1,2

  • 1Jiangsu Key Laboratory of Neuropsychiatric Diseases Research and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, 215021, China.

Cell Death & Disease
|January 11, 2018
PubMed

Insights

MicroRNA miR-3473b exacerbates stroke by increasing neuroinflammation. Inhibiting miR-3473b reduced inflammation and brain damage after stroke in mice, offering a potential therapeutic target.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • MicroRNAs are crucial regulators in biological processes, including stroke pathology.
  • Emerging research highlights the role of specific microRNAs in the complex mechanisms of stroke.
  • Understanding novel microRNAs like miR-3473b is key to developing targeted stroke therapies.

Purpose of the Study:

  • To investigate the role of the newly identified microRNA, miR-3473b, in stroke pathogenesis.
  • To determine the effect of modulating miR-3473b levels on neuroinflammation and infarct volume in a mouse stroke model.
  • To identify the molecular targets and mechanisms through which miR-3473b influences stroke injury.

Main Methods:

  • Transient middle cerebral artery occlusion (MCAO) model in mice to induce ischemic stroke.
  • Intracerebroventricular injection of miR-3473b antagomir to inhibit its activity.
  • In vitro studies using BV2 microglial cells stimulated with lipopolysaccharide (LPS) or conditioned medium from oxygen-glucose deprivation (OGD)-treated neurons.
  • Quantitative real-time PCR, Western blotting, and dual-luciferase reporter assays to measure gene and protein expression and confirm target interaction.

Main Results:

  • miR-3473b expression was significantly upregulated in the cortex and striatum following MCAO.
  • Inhibition of miR-3473b using an antagomir attenuated neuroinflammation and reduced infarct volume in MCAO mice.
  • miR-3473b inhibition decreased pro-inflammatory factors (iNOS, COX-2, TNF-α, IL-6) in vitro and in vivo.
  • Suppressor of cytokine signaling 3 (SOCS3) was identified as a direct target of miR-3473b, with miR-3473b negatively regulating SOCS3 expression.

Conclusions:

  • Upregulation of miR-3473b contributes to stroke pathogenesis by promoting post-stroke neuroinflammation.
  • miR-3473b targets SOCS3, thereby enhancing inflammatory responses in the ischemic brain.
  • Modulating miR-3473b activity, potentially through antagomirs, represents a promising therapeutic strategy for stroke treatment.

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