The SNCA-AS1/miR-138-5p/HIF1A Axis: Implications for diagnosis and cellular pathogenesis in acute cerebral infarction
Pingting Chen1, Yilin Feng2, Cui Bai3
1Department of Neurology, Wenling TCM Hospital Affiliated to Zhejiang Chinese Medical University, Taizhou, 317500, China; First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Background:
Acute cerebral infarction (ACI) is a common cerebrovascular disease with complex pathogenesis. The role of non-coding RNAs in ACI warrants further investigation. To investigate the expression, diagnostic value, and molecular mechanism of SNCA-AS1 in ACI.
Methods:
Blood samples from 125 ACI patients and matched controls were collected. RT-qPCR detected SNCA-AS1, miR-138-5p, and HIF1A expression. ROC curves assessed diagnostic value. BV-2 cells were cultured under oxygen-glucose deprivation (OGD) conditions, with RT-qPCR used to measure molecular expression. Dual-luciferase assays and RNA immunoprecipitation (RIP) were employed to verify the intermolecular interactions within the axis. ELISA determined cytokine levels, CCK-8 and Transwell assays evaluated proliferation and migration, and flow cytometry detected apoptosis. Data were statistically analyzed using t-tests, ANOVA, and correlation analysis.
Results:
SNCA-AS1 and HIF1A were upregulated, while miR-138-5p was downregulated in ACI patients. SNCA-AS1 showed a diagnostic AUC of 0.849. Experiments confirmed SNCA-AS1 binds miR-138-5p and regulates HIF1A. SNCA-AS1 or HIF1A knockdown alleviated inflammation, suppressed proliferation and migration, and promoted apoptosis, effects reversed by miR-138-5p inhibitor.
Conclusion:
SNCA-AS1 participates in ACI pathogenesis through the miR-138-5p/HIF1A axis and may serve as a potential diagnostic marker.
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