MicroRNA152-3p Protects Against Ischemia/Reperfusion-Induced Bbb Destruction Possibly Targeting the MAP3K2/JNK/c-Jun...

Area of Science:

• Neuroscience
• Molecular Biology
• Biochemistry

Background:

• Stroke, particularly ischemic stroke caused by middle cerebral artery occlusion (MCAO), leads to significant neurological deficits.
• Maintaining blood-brain barrier (BBB) integrity is crucial for mitigating ischemic brain injury.
• MicroRNAs (miRNAs) play vital roles in regulating cellular responses to ischemic conditions.

Purpose of the Study:

• To investigate the role of miR-152-3p in protecting against ischemic stroke.
• To elucidate the underlying molecular mechanisms of miR-152-3p's protective effects.

Main Methods:

• Utilized a middle cerebral artery occlusion (MCAO) rat model to induce ischemic stroke.
• Employed an in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model using bEnd.3 cells.
• Assessed neurological deficits, BBB integrity, and endothelial cell apoptosis.
• Investigated the modulation of the MAP3K2/JNK/c-Jun signaling pathway.

Main Results:

• Overexpression of miR-152-3p significantly ameliorated neurological deficits in MCAO rats.
• miR-152-3p levels were decreased in bEnd.3 cells following OGD/R insult.
• Overexpressing miR-152-3p protected bEnd.3 cells from OGD/R-induced microvascular hyperpermeability.
• The protective effect involved negative modulation of the MAP3K2/JNK/c-Jun pathway, leading to reduced endothelial apoptosis.

Conclusions:

• miR-152-3p acts as a protective factor against ischemic stroke.
• Restoring miR-152-3p levels may be a therapeutic strategy for stroke.
• The mechanism involves inhibiting endothelial apoptosis via the MAP3K2/JNK/c-Jun pathway.