Long non‐coding RNA NEAT1 mediates the toxic of Parkinson's disease induced by MPTP/MPP+ via regulation of gene expression. (25th April 2018)

• Record Type: Journal Article
• Authors: Liu, Ying; Lu, Zuneng
• Is Part Of: Clinical and experimental pharmacology and physiology. Volume 45:Number 8(2018)
• Page Start: 841
• Page End: 848
• Publication Date: 2018-04-25
• Subjects: α‐synuclein -- cell line SH‐SY5Y -- NEAT1 -- Parkinson's disease; Clinical pharmacology -- Periodicals; Pharmacology, Experimental -- Periodicals; Physiology, Experimental -- Periodicals; Physiology, Pathological -- Periodicals; 615.1
• DOI: 10.1111/1440-1681.12932
• Languages: English
• ISSNs: 0305-1870

Abstract

Summary: Parkinson's disease (PD) is a result of the loss of dopaminergic neurons in the substantia nigra and is expected to increase the economic burden on patients' families and societies. NEAT1, a long non‐coding RNA, is known as a cancer‐related gene, however, the role of it in PD remains unclear. The aims of this study are to detect the NEAT1‐mediated effects in PD and explore the mechanism of NEAT1 in PD. One group (n = 6) of C57BL/6 model mice were intraperitoneal injected with 1‐Methyl‐4‐phenyl‐2, 3, 6‐tetrahydropyridine (MPTP), while another group (n = 6) was treated with saline and served as control. Human neuroblastoma cell line SH‐SY5Y was pretreated with 1‐Methyl‐4‐phenylpyridinium (MPP+). Cell viability and apoptosis, as well as gene expression with different treatments were examined. Up‐regulated NEAT1 was found in MPTP‐induced PD mice. Moreover, the NEAT1 expression was positively correlated with the concentration of MPP+. In SH‐SY5Y cells stimulated by MPP+, NEAT1 knockdown dramatically promoted cell viability and suppressed cell apoptosis. Additionally, down‐regulation of NEAT1 also decreased the ratio of Bax/Bcl‐2, the activity of caspase‐3, as well as the expression of α‐synuclein. Moreover, α‐synuclein overexpression could significantly reverse the increase in cell viability and the decrease in cell apoptosis induced by NEAT1 knockdown. The results suggested that the knockdown of NEAT1 will have a protective effect on MPTP‐induced PD mice. The mechanism may be related to the dysregulation of α‐synuclein.