헌팅턴병에서 긴 비암호화 리보핵산 발현 분석

헌팅턴병;긴 비암호화 리보핵산;NEAT1;마이크로어레이;Huntington’s disease;long non-coding RNA;microarray;611

자연과학대학 협동과정뇌과학전공 ;

University:서울대학교 대학원

关键词: 헌팅턴병;    긴 비암호화 리보핵산;    NEAT1;    마이크로어레이;    Huntington’s disease;    long non-coding RNA;    microarray;    611;   

Others  :  http://s-space.snu.ac.kr/bitstream/10371/131202/1/000000021016.pdf

美国|英语

来源: Seoul National University Open Repository

【 摘 要 】

Huntington’s disease (HD) is an inherited neurodegenerative disease caused by the abnormal expansion of CAG (cytosine adenine guanine) trinucleotide repeats. Recently attention has focused on long non-coding RNA (lncRNA) which is the most abundant but poorly understood group. An increasing amount of evidence suggests that lncRNAs are involved in a variety of regulatory process, including epigenetic regulation and transcriptional regulation. A small number of studies have reveled clues that lncRNAs are associated with neurodegenerative diseases, but there are few reports regarding genome-wide lncRNA expression change in HD. To discover lncRNAs involved in HD, microarray analysis was performed using caudate nucleus of human brain. A total of 282 lncRNA transcripts were differentially expressed in HD compared with normal control. There were 67 up-regulated lncRNAs and 215 down-regulated lncRNAs, which was consistent in part with previously reported data. Among them upregulation of NEAT1 (nuclear paraspeckle assembly transcript 1) was validated by quantitative reverse transcriptase polymerase chain reaction. Our data demonstrated differential expression of lncRNAs in caudate nucleus of HD, suggesting possibility that dysregulation of lncRNAs accompany neurodegeneration in HD. Further research is needed to assess the functional implication of lncRNAs in HD.