LncRNA HOTAIR promotes MPP+-induced neuronal injury in Parkinson’s disease by regulating the miR-874-5p/ATG10 axis

Authors

  • Jingya Zhao Department of Neurology, Huaihe Hospital of Henan University, Kaifeng 475000, Henan, China
  • Hongli Li Department of Neurology, Huaihe Hospital of Henan University, Kaifeng 475000, Henan, China
  • Na Chang Department of Neurology, Huaihe Hospital of Henan University, No. 115 Ximen Street, Kaifeng 475000, Henan, China. Tel: +86-0371-23906530. E-mail: changnachang1@163.com

DOI:

https://doi.org/10.17179/excli2020-2286

Keywords:

Parkinson’s disease, HOTAIR, miR-874-5p, ATG10, neuronal injury

Abstract

Parkinson’s disease (PD) is a neurodegenerative disease caused by the loss of dopaminergic neurons. Long non-coding RNAs (lncRNAs) play an important role in many neurological diseases, including PD. This study aimed to investigate the role of lncRNA HOX transcript antisense RNA (HOTAIR) in PD pathogenesis and its potential mechanism. SK-N-SH cells were exposed to 1-methyl-4-phenylpyridinium (MPP+) to mimic PD model in vitro. The levels of HOTAIR, miR-874-5p and autophagy-related 10 (ATG10) were determined by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Cell viability and apoptosis were assessed by Cell Counting Kit-8 (CCK-8) assay and flow cytometry. The expression of apoptosis-related proteins was measured by western blot. The levels of neuroinflammation-related factors were detected by enzyme-linked immunosorbent assay (ELISA). Commercial kits was used to monitor lactate dehydrogenase (LDH) activity, reactive oxygen (ROS) generation and superoxide dismutase (SOD) activity. The interaction among HOTAIR, miR-874-5p and ATG10 were verified by dual-luciferase reporter assay or RNA immunoprecipitation (RIP) assay. HOTAIR and ATG10 were up-regulated, and miR-874-5p was down-regulated in dose- and time-dependent manners in MPP+-treated SK-N-SH cells. HOTAIR knockdown reduced MPP+-induced neuronal damage. HOTAIR aggrandized MPP+-triggered neuronal injury by sponging miR-874-5p. Also, miR-874-5p attenuated MPP+-triggered neuronal damage by targeting ATG10. Moreover, HOTAIR regulated ATG10 expression via sponging miR-874-5p. HOTAIR promoted MPP+-induced neuronal injury via modulating the miR-874-5p/ATG10 axis in SK-N-SH cells.

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Published

2020-08-05

How to Cite

Zhao, J., Li, H., & Chang, N. (2020). LncRNA HOTAIR promotes MPP+-induced neuronal injury in Parkinson’s disease by regulating the miR-874-5p/ATG10 axis. EXCLI Journal, 19, 1141–1153. https://doi.org/10.17179/excli2020-2286

Issue

Vol. 19 (2020)

Section

Original articles

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Copyright (c) 2020 Jingya Zhao, Hongli Li, Na Chang

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