期刊
MOLECULAR NEUROBIOLOGY
卷 54, 期 2, 页码 1577-1586出版社
HUMANA PRESS INC
DOI: 10.1007/s12035-016-9928-9
关键词
Huntington's disease; Long noncoding RNA NEAT1; Microarray; Neuroprotection
资金
- Korean Health Technology RD Project [HI14C2348, HI12C1773]
- Ministry of Health and Welfare, Republic of Korea
- National Research Foundation (NRF) of Korea [2011-0012728]
- Seoul National University Hospital Research Fund [04-2014-0730]
Huntington's disease (HD) is a devastating neurodegenerative disease caused by cytosine-adenine-guanine trinucleotide repeat expansion in the huntingtin gene. Growing evidence supports the regulatory functions of long noncoding RNAs (lncRNAs) in the disease process, but little is known about the association between lncRNAs and neuronal death in HD. Here, we evaluated the altered expression profiles of lncRNA in HD by using microarrays. Among dysregulated lncRNAs, we focused on the upregulation of nuclear paraspeckle assembly transcript 1 (NEAT1). Quantitative PCR analysis validated increased NEAT1 levels in the R6/2 mouse brain as well as the human HD postmortem brain. To determine the biological effects of NEAT1 on neuronal survival, neuro2A cells were transfected with the NEAT1 short isoform vector and were subjected to H2O2-induced injury. Subsequently, NEAT1-transfected cells showed increased viability under oxidative stress. Our observations support the notion that NEAT1 upregulation in HD contributes to the neuroprotective mechanism against neuronal injury rather than the pathological process underlying neurodegeneration in HD.
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