LincRNA-p21 Inhibits Cell Viability and Promotes Cell Apoptosis in Parkinson's Disease through Activating α-Synuclein Expression. (25th December 2018)

• Record Type: Journal Article
• Authors: Xu, Xiaonan; Zhuang, Chengle; Wu, Zimu; Qiu, Hongyan; Feng, Haixia; Wu, Jun
• Other Names: Surguchov Andrei Academic Editor.
• Is Part Of: BioMed research international. Volume 2018(2018)
• Publication Date: 2018-12-25
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2018/8181374
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : 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.