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MiR-92a-3p regulates microglial autophagy and inflammation after intracerebral hemorrhage via ATG14
Lin Yao1, Qian He1, Shengyun Hao1
1Department of General Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
Background:
Intracerebral hemorrhage (ICH) is a prevalent cerebrovascular event that triggers secondary brain injury in which microglial activation is central. This study explored how miR-92a-3p governs autophagy and inflammatory signaling in this context.
Methods:
An in vitro ICH model was established using rat microglia exposed to hemoglobin, with lipopolysaccharide to induce autophagy. Cells were transfected with miR-92a-3p mimics or inhibitors. Apoptosis, miR-92a-3p/ATG14 expression, autophagy-related proteins (LC3, P62), and pro-inflammatory factors were assessed via molecular and cellular assays.
Results:
Dual luciferase assays and ATG14 silencing confirmed direct targeting of ATG14 by miR-92a-3p. Upregulation of miR-92a-3p suppressed autophagy and thereby reduced inflammatory cytokine release, whereas inhibition of miR-92a-3p restored autophagic activity and reduced inflammation.
Conclusion:
These findings establish miR-92a-3p as a critical regulator of microglial autophagy and inflammation after hemorrhagic stroke and identify it as a prospective therapeutic target for neuroinflammatory modulation.
Insights
Microglial activation in intracerebral hemorrhage (ICH) involves miR-92a-3p regulating autophagy and inflammation. This microRNA suppresses autophagy, reducing inflammatory cytokine release, offering a therapeutic target for hemorrhagic stroke.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Intracerebral hemorrhage (ICH) is a common stroke type causing secondary brain injury.
- Microglial activation plays a key role in the inflammatory response following ICH.
- MicroRNAs are increasingly recognized as critical regulators in neurological diseases.
Purpose of the Study:
- To investigate the role of miR-92a-3p in regulating microglial autophagy and inflammation after ICH.
- To determine the molecular mechanism by which miR-92a-3p influences autophagic and inflammatory pathways in microglia.
Main Methods:
- An in vitro model of ICH was created using rat microglia exposed to hemoglobin.
- Cells were treated with lipopolysaccharide to induce autophagy and transfected with miR-92a-3p mimics or inhibitors.
- Apoptosis, gene/protein expression (miR-92a-3p, ATG14, LC3, P62), and inflammatory factors were analyzed.
Main Results:
- miR-92a-3p directly targets ATG14, a crucial autophagy-related gene.
- Upregulation of miR-92a-3p inhibited autophagy and decreased the release of inflammatory cytokines.
- Inhibition of miR-92a-3p restored autophagic activity and reduced inflammation.
Conclusions:
- miR-92a-3p is a key regulator of microglial autophagy and inflammation in the context of hemorrhagic stroke.
- Targeting miR-92a-3p presents a potential therapeutic strategy for modulating neuroinflammation.
- This study elucidates a novel mechanism linking microRNA regulation to autophagy and inflammation in ICH.
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