Wang Xinhua, Zhang Min, Liu Hengfang
a Department of Neurology , The Fifth Affiliated Hospital of Zhengzhou University , Zhengzhou , Henan Province , China.
Biosci Biotechnol Biochem. 2019 Apr;83(4):609-621. doi: 10.1080/09168451.2018.1562874. Epub 2019 Jan 17.
Considerable evidence suggest that a variety of Long-non-coding RNAs (LncRNAs) are widely implicated in several neurodegenerative disorders. The present study aims to investigate the regulatory effect of LncRNA 17A in an in vitro model of Alzheimer's disease (AD). AD cell model was established by treating the SH-SY5Y cells with amyloid β peptide 1-42, and then the cells were transfected with 17A shRNA and pcDNA-17A. Apoptosis, migration, invasion and ELISA assays were performed to investigate the effect of differentiated 17A expression level on AD cell line. It was determined that 17A-overexpressing promotes autophagy, induces neurodegenration and deactivates GABAB signaling. In conclusion, our results demonstrated that the dysregulation of LncRNA 17A was involved in cellular functions and biological processes of neuroblastoma cells in an AD cell model, shedding light on the diagnostic value and therapeutic potential of LncRNA 17A for AD intervention.
大量证据表明，多种长链非编码RNA（LncRNAs）广泛参与多种神经退行性疾病。本研究旨在探讨LncRNA 17A在阿尔茨海默病（AD）体外模型中的调控作用。用淀粉样β肽1-42处理SH-SY5Y细胞建立AD细胞模型，然后用17A shRNA和pcDNA-17A转染细胞。进行凋亡、迁移、侵袭和ELISA检测，以研究17A表达水平差异对AD细胞系的影响。结果表明，过表达17A可促进自噬、诱导神经退变并使GABAB信号失活。总之，我们的结果表明，LncRNA 17A的失调参与了AD细胞模型中神经母细胞瘤细胞的细胞功能和生物学过程，为LncRNA 17A在AD干预中的诊断价值和治疗潜力提供了线索。
