MicroRNA‑634 alters nerve apoptosis via the PI3K/Akt pathway in cerebral infarction

Area of Science:

• Neuroscience
• Molecular Biology
• Biochemistry

Background:

• Cerebral infarction, a major cause of disability, involves nerve inflammation and apoptosis.
• The precise molecular mechanisms regulating these processes remain incompletely understood.

Purpose of the Study:

• To investigate the role and mechanism of microRNA-634 (miRNA-634) in nerve inflammation and apoptosis during cerebral infarction.
• To explore the potential of miRNA-634 as a therapeutic target.

Main Methods:

• Establishment of a cerebral infarction rat model and an in vitro cell model.
• Analysis of miRNA-634 expression levels.
• Investigation of the effects of miRNA-634 modulation on cell apoptosis and protein expression (caspase-3, Bax).
• Exploration of the involvement of the phosphoinositide 3-kinase (PI3K)/Akt pathway using inhibitors and agonists.

Main Results:

• miRNA-634 expression was upregulated in cerebral infarction models.
• Upregulated miRNA-634 increased cell apoptosis and caspase-3/Bax protein expression by inactivating the PI3K/Akt pathway.
• Downregulated miRNA-634 promoted cell growth and inhibited apoptosis via PI3K/Akt pathway induction.
• PI3K inhibition reversed the effects of miRNA-634 downregulation, while a PI3K agonist counteracted miRNA-634 upregulation effects.

Conclusions:

• miRNA-634 plays a critical role in regulating nerve inflammation and apoptosis in cerebral infarction.
• The PI3K/Akt pathway is a key mediator of miRNA-634's effects.
• miRNA-634 represents a potential therapeutic target for cerebral infarction treatment.