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Long non-coding RNA MEG3 promotes cerebral ischemia-reperfusion injury through increasing pyroptosis by targeting

Ji Liang1, Qiang Wang1, Jun-Qi Li1

  • 1Department of Neurology, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou 570208, Hainan Province, PR China.

Experimental Neurology
|December 4, 2019
PubMed
Abstract

Insights

Long non-coding RNA MEG3 promotes ischemic stroke by activating the AIM2 inflammasome. This pathway involves MEG3 sponging miR-485, which targets AIM2, leading to pyroptosis and inflammation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Inflammasomes, particularly AIM2, are implicated in ischemic brain injury.
  • Pyroptosis and inflammation are key pathological processes in cerebral ischemia/reperfusion (I/R).
  • Long non-coding RNAs (lncRNAs) are emerging as critical regulators in various biological processes, including neurological disorders.

Purpose of the Study:

  • To elucidate the regulatory mechanism of lncRNA MEG3 on the AIM2 inflammasome in cerebral I/R.
  • To investigate the role of the MEG3/miR-485/AIM2 axis in pyroptosis and inflammation during cerebral I/R.

Main Methods:

  • Established in vivo (MCAO) and in vitro (OGD/R) models of cerebral I/R.
  • Assessed ischemic injury using TTC, H&E, and TUNEL assays.
  • Quantified gene and protein expression of MEG3, miR-485, AIM2, and inflammasome components via qRT-PCR, IHC, immunofluorescence, ELISA, and Western blotting.
  • Validated interactions using dual luciferase reporter and Ago2-RIP assays.

Main Results:

  • MEG3 and AIM2 were upregulated, while miR-485 was downregulated in cerebral I/R models.
  • MEG3 acted as a molecular sponge for miR-485, and AIM2 was a direct target of miR-485.
  • MEG3 knockdown reduced OGD/R-induced pyroptosis and inflammation by inhibiting caspase-1 signaling and AIM2 expression.

Conclusions:

  • The MEG3/miR-485/AIM2 axis promotes pyroptosis via caspase-1 activation in cerebral I/R.
  • This axis represents a potential therapeutic target for ischemic stroke.
Keywords:
AIM2Cerebral ischemia-reperfusion injuryMEG3PyroptosismiR-485

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