LincRNA-p21 Inhibits Cell Viability and Promotes Cell Apoptosis in Parkinson’s Disease through Activating α-Synuclein Expression

Long intergenic noncoding RNA-p21 (lincRNA-p21) has been reported to be increased in Parkinson’s disease (PD). However, the function and underlying mechanisms of lincRNA-p21 remain not clear. In order to explore the role of lincRNA-p21 in PD, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPT...

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Bibliographic Details
Published in:BioMed research international 2018, Vol.2018 (2018), p.1-10
Main Authors: Feng, Haixia, Qiu, Hongyan, Wu, Zimu, Zhuang, Chengle, Xu, Xiaonan, Wu, Jun
Format: Article
Language:English
Subjects:
Animal models
Apoptosis
Binding sites
Biomedical research
Cyclin-dependent kinase inhibitor p21
Experiments
Gene expression
Laboratory animals
MicroRNAs
Movement disorders
MPP
MPTP
Neurodegenerative diseases
Neurology
Parkinson's disease
Plasmids
Ribonucleic acid
RNA
Stem cells
Synuclein
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Summary:Long intergenic noncoding RNA-p21 (lincRNA-p21) has been reported to be increased in Parkinson’s disease (PD). However, the function and underlying mechanisms of lincRNA-p21 remain not clear. In order to explore the role of lincRNA-p21 in PD, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce in vivo PD model (C57BL/6 mice) and utilized N-methyl-4-phenylpyridinium (MPP+) to create in vitro PD model (SH-SY5Y cells). Results showed that the expression level of lincRNA-p21 was increased significantly in PD models. High abundance of lincRNA-p21 inhibited viability and promoted apoptosis markedly in SH-SY5Y cells treated with MPP+. Mechanistically, further experiments demonstrated that upregulation of lincRNA-p21 could sponge miR-1277-5p and indirectly increase the expression of α-synuclein to suppress viability and activate apoptosis in SH-SY5Y cells. In short, our study illustrated that lincRNA-p21/miR-1277-5p axis regulated viability and apoptosis in SH-SY5Y cells treated with MPP+ via targeting α-synuclein. LincRNA-p21 might be a novel target for PD.
ISSN:2314-6133
2314-6141
DOI:10.1155/2018/8181374