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연세대학교 의과대학 Yonsei Medical Journal Yonsei Medical Journal 제60권 제7호
발행연도
2019.1
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640 - 650 (11page)

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Purpose: Alzheimer’s disease (AD) is the most common neurodegenerative disease, with a rising prevalence worldwide. Longnoncoding RNAs (lncRNAs) have been found to play important roles in the development and treatment of AD. However, the exactrole of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in neuronal damage in AD is largely unknown. Materials and Methods: The AD model was established in SH-SY5Y and SK-N-SH cells via treatment with amyloid β1-42 (Aβ). Theexpression of NEAT1 and microRNA-107 (miR-107) was measured by quantitative real-time polymerase chain reaction. Cell viabilityand apoptosis were detected by MTT assay, immunocytochemistry, and flow cytometry. The expression of phosphorylated tauprotein (p-Tau) was measured by Western blot. The interaction between NEAT1 and miR-107 was explored by bioinformaticsanalysis, luciferase activity, and RNA immunoprecipitation assays. Results: NEAT1 expression was enhanced in Aβ-treated SH-SY5Y and SK-N-SH cells, and its knockdown attenuated Aβ-inducedinhibition of viability and promotion of apoptosis and p-Tau levels. NEAT1 was indicated as a decoy of miR-107. miR-107 abundancewas reduced in Aβ-treated cells, and its overexpression reversed Aβ-induced injury. Moreover, interference of miR-107 abatedsilencing of NEAT1-mediated inhibition of neuronal damage in Aβ-treated SH-SY5Y and SK-N-SH cells. Conclusion: LncRNA NEAT1 aggravated Aβ-induced neuronal damage by sponging miR-107, indicating a novel avenue for treatmentof AD.

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