Abstract
Aims: In this study, the authors hypothesized that, in an in vitro Alzheimer's disease model, the epigenetic axis of SNHG19/hsa-miR-137 functionally regulates amyloid beta peptide 25-35 (Aβ25-35)-induced SH-SY5Y cytotoxicity. Methods: Dual luciferase activity assay demonstrated that SNHG19 could directly bind hsa-miR-137. In Aβ25-35-treated SH-SY5Y cells, SNHG19 was upregulated and hsa-miR-137 downregulated. Results: SNHG19 knockdown ameliorated Aβ25-35-induced SH-SY5Y cytotoxicity, then reversed by secondary hsa-miR-137 downregulation. TNFAIP1 was dynamically regulated by Aβ25-35 and gene modifications in SH-SY5Y cells. Finally, upregulation of TNFAIP1 reversed the protective effect of SNHG19 knockdown on Aβ25-35-induced cytotoxicity. Conclusions: The authors concluded that the epigenetic axis of SNHG19/hsa-miR-137/TNFAIP1 may functionally regulate Aβ25-35-induced SH-SY5Y cytotoxicity, thus making it a potential molecular target for Alzheimer's disease treatment.
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