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Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
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Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury

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METTL14 regulates microglia/macrophage polarization and NLRP3 inflammasome activation after ischemic stroke by the

Yamei Li1, Jiacen Li2, Qian Yu1

  • 1Department of Rehabilitation Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, Sichuan, China.

Neurobiology of Disease
|August 4, 2023
PubMed

Insights

Methyltransferase-like 14 (METTL14) promotes ischemic stroke brain injury by upregulating M1 microglia polarization and the NLRP3 inflammasome/pyroptosis axis. METTL14 depletion alleviates injury by inhibiting these pathways.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • N6-methyladenosine (m6A) is vital in ischemic stroke.
  • The specific role of methyltransferase-like 14 (METTL14) in ischemic stroke is currently unknown.

Purpose of the Study:

  • To investigate the role of METTL14 in ischemic stroke.
  • To elucidate the underlying molecular mechanisms of METTL14 in brain injury.

Main Methods:

  • In vivo middle cerebral artery occlusion (MCAO) rat model.
  • In vitro oxygen-glucose deprivation/reperfusion (OGD/R) in HAPI cells.
  • Analysis of METTL14, KAT3B, STING, and H3K27ac expression and modification.

Main Results:

  • METTL14 expression was upregulated in microglia/macrophages post-MCAO and OGD/R.
  • METTL14 enhanced KAT3B expression via m6A modification of KAT3B mRNA.
  • KAT3B increased STING expression by enhancing H3K27ac at the STING promoter.
  • METTL14 promoted M1 polarization and the NLRP3 inflammasome/pyroptosis axis through the KAT3B-STING pathway.
  • METTL14 depletion reduced brain injury in MCAO rats by inhibiting M1-like microglia/macrophage polarization and the NLRP3 inflammasome/pyroptosis axis.

Conclusions:

  • METTL14 depletion alleviates MCAO-induced brain injury.
  • METTL14 likely shifts microglia/macrophage polarization from M1 to M2.
  • METTL14 depletion restrains the NLRP3 inflammasome/pyroptosis axis in microglia/macrophages.
Keywords:
Ischemic strokeMETTL14Microglial polarizationNLRP3 inflammasome

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