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Long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) sponges microRNA-124-3p to up-regulate phosphodiesterase 4B (PDE4B) to accelerate the progression of Parkinson's disease.

Authors
  • Chen, Ming-Yu1
  • Fan, Kai2
  • Zhao, Lian-Jiang2
  • Wei, Jie-Mei1
  • Gao, Ji-Xu3
  • Li, Zhen-Fu1
  • 1 Department of Neurology, Linyi Central Hospital, Linyi City Shandong, China. , (China)
  • 2 Department of Neurology, The Third People's Hospital of Linyi, Linyi City Shandong, China. , (China)
  • 3 Department of Laboratory, Linyi Cancer Hospital, Linyi City Shandong, China. , (China)
Type
Published Article
Journal
Bioengineered
Publisher
Landes Bioscience
Publication Date
Dec 01, 2021
Volume
12
Issue
1
Pages
708–719
Identifiers
DOI: 10.1080/21655979.2021.1883279
PMID: 33522352
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Reportedly, long non-coding RNA (lncRNA) are crucial modulators in neurodegenerative diseases. Herein, we investigated the role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in Parkinson's disease (PD). In-vitro PD model was established based on SH-SY5Y cells treated with 1-methyl-4-phenylpyridinium (MPP+). NEAT1, microRNA (miR) -124-3p and phosphodiesterase 4B (PDE4B) expression levels were examined by qRT-PCR. CCK-8 assay and LDH release assay were adopted to delve into the cell viability and cytotoxicity, respectively. Besides, western blot was utilized to determine mTOR, p-mTOR and PDE4B expression levels. ELISA was executed to detect the levels of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and interleukin 6 (IL-6). Dual-luciferase reporter assay and RIP assay were used to probe the relationship between miR-124-3p and NEAT1 or PDE4B. We demonstrated that, in SH-SY5Y cells treated with MPP+, NEAT1 and PDE4B expression levels were raised, while miR-124-3p expression was repressed; NEAT1 depletion or miR-124-3p overexpression increased the cell viability and suppressed cell injury. Besides, miR-124-3p was confirmed as the direct target of NEAT1, and its down-regulation counteracted the impact of NEAT1 depletion on SH-SY5Y cells. PDE4B was as the downstream target of miR-124-3p, and its overexpression weakens the impact of miR-124-3p on SH-SY5Y cells. Additionally, NEAT1 decoyed miR-124-3p to modulate PDE4B expression. Collectively, in MPP+-induced SH-SY5Y cells, NEAT1 depletion increases cell viability, represses cytotoxicity and reduces inflammatory response by regulating miR-124-3p and PDE4B expression levels, suggesting that NEAT1 may be a promising target for treating PD.

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