LincRNA-p21 Inhibits Cell Viability and Promotes Cell Apoptosis in Parkinson’s Disease through Activating<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mtext mathvariant="bold">α</mml:mtext></mml:mrow></mml:math>-Synuclein Expression

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 <i>in vivo</i> PD model (C57BL/6 mice) and utilized N-methyl-4-phenylpyridinium (MPP⁺) to create <i>in vitro</i> 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 <i>α</i>-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 <i>α</i>-synuclein. LincRNA-p21 might be a novel target for PD.