Abstract
Accumulating evidence suggests that dysregulation of long non-coding RNAs is closely associated with various human diseases, including Parkinson’s disease (PD). However, the role of nuclear-enriched abundant transcript 1 (NEAT1) in the PD process remains unclear. The number of TH+ cells was reduced, and the expression levels of NEAT1 and Krüppel-like factor 4 (KLF4) were increased in the midbrain of MPTP-HCl-treated mice. In addition, the expression of cleaved-caspase-3 (cleaved-casp-3) and Bax (apoptosis-related proteins) was increased, while the expression of Bcl-2 (anti-apoptotic protein) was reduced in MPTP-HCl-treated mice. The expression levels of NEAT1 and KLF4 were increased in MPP+-treated SH-SY5Y cells. Knockdown of NEAT1 promoted cell viability and decreased apoptosis in MPP+-treated SH-SY5Y cells, which could be reversed by upregulating KLF4. KLF4 was verified as a direct target of miR-124, and miR-124 could particularly bind to NEAT1. Downregulation of NEAT1 significantly increased cell viability and decreased apoptosis by regulating miR-124 expression in MPP+-treated SH-SY5Y cells. Additionally, interference of NEAT1 increased the number of TH+ cells and miR-124 expression, while reduced apoptosis and expression of KLF4 in vivo. NEAT1 knockdown increased cell viability and suppressed apoptosis in PD via regulating the miR-124/KLF4 axis, providing a promising avenue for the treatment of PD.
Highlights
Parkinson’s disease (PD) is the second most common multifactorial neurodegenerative disease, and it is estimated to affect 7–10 million people worldwide, especially older adults [1]
In order to detect the number of TH+ cells and the expression of nuclear-enriched abundant transcript 1 (NEAT1) and Krüppel-like factor 4 (KLF4) in the brain of MPTPtreated mice (n = 7), MPTP–HCl was injected into a group of mice, and a sterile saline solution (0.9%) was injected into the control group
The results of Quantitative reverse transcriptionpolymerase chain reaction (qRT-PCR) showed that NEAT1 and KLF4 expression levels were upregulated in the midbrain of PD mice (P < 0.05, Figure 1b and c)
Summary
Parkinson’s disease (PD) is the second most common multifactorial neurodegenerative disease, and it is estimated to affect 7–10 million people worldwide, especially older adults [1]. Statistics show that the incidence of PD continues to increase, and the trend is relatively young [2,3]. PD is caused by the loss of dopaminergic neurons in the substantia nigra, striatum and cerebral cortex. The main symptoms include bradykinesia, stiffness, resting tremor and unstable posture [4,5]. Due to complex causes and mechanisms, the current treatments, including drugs and surgery, can only reduce the symptoms of PD but cannot inhibit the development of PD.
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