首页|MiR-141-3p Expression Profiling in MPP Treated Differentiated SH-SY5Y Cells: A Model of Parkinson's Disease
MiR-141-3p Expression Profiling in MPP Treated Differentiated SH-SY5Y Cells: A Model of Parkinson's Disease
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NSTL
Springer Nature
Parkinson's disease is known as the second most common neurodegenerative disorder that commonly affects the older population. MicroRNAs are categorized as short non-coding RNAs (19-24 nt) involved in the post-transcriptional regulation of gene expression in multicellular organisms. They can influence both stability and translation of mRNAs. Recent studies suggested that miR-141 which is well-known in oxidative-stress pathway is up-regulated in some neurodegenerative diseases including the Alzheimer disease. This study was intended to evaluate the miR-141 expression and its predicted target gene in the MPP+ treated differentiated SH-SY5Y cells. In silico studies were also considered by using miRWalk and TargetScan databases to determinate any possible target of miR-141. Moreover, SHSY-5Y cells were allowed to be exposed to MPP+ as a parkinsonian neurotoxin. The quantification of the expression levels of miR-141 and the predicted target mRNA was done by using RT-qPCR to show their expression pattern. Results showed the significant up-regulation of miR-141 during the treatment of human SH-SY5Y cells with MPP+, inducing oxidative stress and apoptosis. Furthermore, transcript level of SIRT1 in these cells exhibited significant down-regulation under MPP+ treatment. In addition, exposure to MPP+ raised the apoptotic rate, leading to ROS accumulation and oxidative stress. To summarize, it was found that miR-141 expression could trigger the PD-related pathogenic processes and decreased SIRT1 expression is associated with increased miR-141 expression in MPP+ treated SHSY-5Y cells.
in silico analysismiR-141SH-SY5YSIRT1Parkinson's diseaseALZHEIMERS-DISEASEMPTPNEURONSGENEN-METHYL-4-PHENYLPYRIDINENEURODEGENERATIONDEATH
Ghaedi, Kamran、Peymani, Maryam、Esfahani, Mohammad Hossein Nasr、Dana, Shadab
NSTL
Springer Nature
