LINC01094 exacerbates acute cerebral infarction by regulating miR-499a-5p.

Area of Science:

• Molecular Biology
• Neuroscience
• Genetics

Background:

• Acute cerebral infarction (ACI) is a major cause of disability and mortality.
• The molecular mechanisms underlying ACI pathogenesis remain incompletely understood.
• Long non-coding RNAs (lncRNAs) are emerging as critical regulators in various diseases, including neurological disorders.

Purpose of the Study:

• To investigate the role of lncRNA LINC01094 in the pathological process of ACI.
• To explore the potential molecular mechanisms involving LINC01094 in ACI.
• To evaluate LINC01094 as a potential diagnostic biomarker and therapeutic target for ACI.

Main Methods:

• Quantitative real-time PCR (RT-qPCR) to measure gene expression.
• Biochemical assays to assess oxidative stress markers (MDA, SOD, ROS).
• Cell viability (CCK-8) and apoptosis assays (flow cytometry).
• Dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) assays to validate molecular interactions.
• Animal models (MCAO rats) and in vitro models (OGD/R in SH-SY5Y cells).

Main Results:

• Serum LINC01094 expression was significantly upregulated in ACI patients and showed diagnostic value.
• LINC01094 expression was negatively correlated with miR-499a-5p levels in ACI patients.
• Downregulation of LINC01094 protected against cerebral injury in vitro and in vivo models.
• Inhibition of miR-499a-5p reversed the protective effects of LINC01094 downregulation.
• CACNB2 was identified as a direct target of miR-499a-5p.

Conclusions:

• LINC01094 plays a crucial role in promoting ACI pathogenesis by sponging miR-499a-5p.
• LINC01094 acts as a competing endogenous RNA (ceRNA) to regulate miR-499a-5p/CACNB2 axis.
• LINC01094 represents a promising diagnostic biomarker and therapeutic target for ACI.