Integrated transcriptome expression profiling reveals a novel lncRNA associated with L-DOPA-induced dyskinesia in a rat model of Parkinson’s disease
Author(s) -
Chunlei Han,
Yunpeng Liu,
YunPeng Sui,
Ning Chen,
Tingting Du,
Ying Jiang,
Chenjia Guo,
Kailiang Wang,
Qiao Wang,
Shiying Fan,
Shimabukuro Michitomo,
Fangang Meng,
Yuan Fang,
Jianguo Zhang
Publication year - 2020
Publication title -
aging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 90
ISSN - 1945-4589
DOI - 10.18632/aging.102652
Subject(s) - dyskinesia , transcriptome , biology , long non coding rna , gene expression , parkinson's disease , gene , rna , microbiology and biotechnology , blot , gene expression profiling , disease , genetics , medicine
Levodopa-induced dyskinesia (LID) is a common complication of chronic dopamine replacement therapy in the treatment of Parkinson's disease (PD). Long noncoding RNAs regulate gene expression and participate in many biological processes. However, the role of long noncoding RNAs in LID is not well understood. In the present study, we examined the lncRNA transcriptome profile of a rat model of PD and LID by RNA sequence and got a subset of lncRNAs, which were gradually decreased during the development of PD and LID. We further identified a previously uncharacterized long noncoding RNA, NONRATT023402.2, and its target genes glutathione S-transferase omega (Gsto) 2 and prostaglandin E receptor ( Ptger )3. All of them were decreased in the PD and LID rats as shown by quantitative real-time PCR, fluorescence in situ hybridization and western blotting. Pearson's correlation analysis showed that their expression was positively correlated with the dyskinesia score of LID rats. In vitro experiments by small interfering RNA confirmed that slicing NONRATT023402 inhibited Gsto2 and Ptger3 and promoted the inflammatory response. These results demonstrate that NONRATT023402.2 may have inhibitive effects on the development of PD and LID.
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