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Hemoglobin enhances miRNA-144 expression and autophagic activation mediated inflammation of microglia via mTOR

Zhenyu Wang1, Bangqing Yuan2, Fenlan Fu2

  • 1Department of rehabilitation medicine, Yongchuan Hospital, Chongqing Medical University, Chongqing, 402160, China.

Scientific Reports
|September 21, 2017
PubMed

Insights

Intracerebral hemorrhage activates microglia via miRNA-144, promoting inflammation. This microRNA targets mTOR, suggesting a new therapeutic approach for brain hemorrhage by modulating this pathway.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Intracerebral hemorrhage (ICH) triggers microglial autophagy and neuroinflammation.
  • MicroRNAs (miRNAs) regulate autophagy posttranscriptionally, but specific miRNAs in ICH-induced microglial autophagy are unknown.

Purpose of the Study:

  • To identify specific miRNAs involved in ICH-mediated microglial autophagic activation.
  • To elucidate the regulatory pathway of identified miRNAs in microglia.

Main Methods:

  • Microglia were treated with hemoglobin (Hb).
  • miRNA-144 expression, autophagic activation, and inflammation were measured.
  • The mechanistic target of rapamycin (mTOR) was identified as a target of miRNA-144.

Main Results:

  • Hemoglobin exposure increased miRNA-144 expression and induced autophagic activation and inflammation in microglia.
  • miRNA-144 directly targets the 3' UTR of mTOR, regulating its function.
  • Overexpression of mTOR attenuated the autophagic activation and inflammation.

Conclusions:

  • miRNA-144 mediates hemoglobin-induced microglial autophagic activation and inflammation through the mTOR pathway.
  • miRNA-based therapies offer a potential strategy for treating intracerebral hemorrhage.

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