Altered Expression of the Long Noncoding RNA NEAT1 in Huntington's Disease

被引：124

作者：

Sunwoo, Jun-Sang ^{[1
,2
,3
]}

Lee, Soon-Tae ^{[1
,2
]}

Im, Wooseok ^{[1
,2
]}

Lee, Mijung ^{[1
,2
]}

Byun, Jung-Ick ^{[1
,2
,4
]}

Jung, Keun-Hwa ^{[1
,2
]}

Park, Kyung-Il ^{[5
]}

Jung, Ki-Young ^{[1
,2
]}

Lee, Sang Kun ^{[1
,2
]}

Chu, Kon ^{[1
,2
]}

Kim, Manho ^{[1
,2
,6
]}

机构：

[1] Seoul Natl Univ Hosp, Biomed Res Inst, Dept Neurol, Lab Neurotherapeut, Seoul 03080, South Korea

[2] Seoul Natl Univ, Coll Med, Program Neurosci, Seoul, South Korea

[3] Soonchunhyang Univ, Sch Med, Dept Neurol, Seoul, South Korea

[4] Kyung Hee Univ Hosp Gangdong, Dept Neurol, Seoul, South Korea

[5] Seoul Natl Univ Hosp, Dept Neurol, Healthcare Syst Gangnam Ctr, Seoul, South Korea

[6] Seoul Natl Univ, Coll Med, Prot Metab Med Res Ctr, Seoul, South Korea

来源：

MOLECULAR NEUROBIOLOGY | 2017年 / 54卷 / 02期

基金：

新加坡国家研究基金会;

关键词：

Huntington's disease; Long noncoding RNA NEAT1; Microarray; Neuroprotection; ALZHEIMERS-DISEASE; MUTANT HUNTINGTIN; STRIATAL CELLS; STEM-CELLS; DYSFUNCTION; REPEAT; MODELS; GENE; ABNORMALITIES; PROGRESSION;

D O I：

10.1007/s12035-016-9928-9

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：1577 / 1586

页数：10

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