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Long non‐coding RNA NEAT 1 mediates the toxic of Parkinson's disease induced by MPTP / MPP + via regulation of gene expression
Author(s) -
Liu Ying,
Lu Zuneng
Publication year - 2018
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12932
Subject(s) - mptp , gene knockdown , viability assay , apoptosis , substantia nigra , chemistry , dopaminergic , cell , gene expression , microbiology and biotechnology , pharmacology , biology , gene , endocrinology , biochemistry , dopamine
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. NEAT 1, 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 NEAT 1‐mediated effects in PD and explore the mechanism of NEAT 1 in PD . One group (n = 6) of C57 BL /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 ‐ SY 5Y was pretreated with 1‐Methyl‐4‐phenylpyridinium ( MPP +). Cell viability and apoptosis, as well as gene expression with different treatments were examined. Up‐regulated NEAT 1 was found in MPTP ‐induced PD mice. Moreover, the NEAT 1 expression was positively correlated with the concentration of MPP +. In SH ‐ SY 5Y cells stimulated by MPP +, NEAT 1 knockdown dramatically promoted cell viability and suppressed cell apoptosis. Additionally, down‐regulation of NEAT 1 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 NEAT 1 knockdown. The results suggested that the knockdown of NEAT 1 will have a protective effect on MPTP ‐induced PD mice. The mechanism may be related to the dysregulation of α‐synuclein.