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Mir-141-3p Regulates Apoptosis and Mitochondrial Membrane Potential via Targeting Sirtuin1 in a 1-Methyl-4-Phenylpyridinium in vitro Model of Parkinson’s Disease
المؤلفون المشاركون
Zheng, Yumin
Dong, Li
Liu, Na
Luo, Xiaoguang
He, Zhiyi
المصدر
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-14، 14ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-11-07
دولة النشر
مصر
عدد الصفحات
14
التخصصات الرئيسية
الملخص EN
Objectives.
Parkinson’s disease (PD) is a common neurodegenerative disease characterized by the loss of midbrain dopaminergic neurons in the substantia nigra.
The present study investigated miR-141-3p/sirtuin1 (SIRT1) activity in a 1-methyl-4-phenylpyridinium- (MPP+-) induced PC12-cell model of PD.
Methods.
PC12 cells were exposed to MMP+ following induction of differentiation by nerve growth factor (NGF).
miR-141-3p and SIRT1 expressions were examined using RT-qPCR and western blot.
Cell viability was evaluated using the MTT assay.
Apoptosis percentage, reactive oxygen species (ROS) production, and mitochondrial membrane potential (Δψm) were evaluated using flow cytometry.
Expression of Nuclear factor-kappa B- (NF-κB-) related proteins was determined by western blot.
Bioinformatic analysis, RT-qPCR, and luciferase reporter assay were used to confirm the interaction between miR-141-3p and SIRT1.
Results.
miR-141-3p was upregulated, and SIRT1 was downregulated in MPP+-treated PC12 cells.
MPP+ treatment also upregulated nitric oxide synthase 1 (Nos1) and α-synuclein.
miR-141-3p induced apoptosis, oxidative stress, mitochondrial dysfunction, and downregulated the SIRT1 mRNA expression.
The luciferase reporter assay showed that SIRT1 was the target of miR-141-3p.
SIRT1 transfection attenuated apoptosis, ROS production and maintained Δψm.
SIRT1 also downregulated Nos1, tumor necrosis factor-α (TNF-α), interleukin 1 beta (IL-1β), interleukin 6(IL-6) and upregulated B cell lymphoma 2 (Bcl-2) protein.
In addition, SIRT1 activator resveratrol blocked the effects of miR-141-3p mimic on Nos1, α-synuclein, and mitochondrial membrane potential.
SIRT1 inhibitor sirtinol reversed the biological effects of miR-141-3p.
Conclusion.
Increased miR-141-3p induced apoptosis, oxidative stress, and mitochondrial dysfunction in MPP+-treated PC12 cells by directly targeting the SIRT1 expression.
Our study provided a potential therapeutic strategy for PD.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Zheng, Yumin& Dong, Li& Liu, Na& Luo, Xiaoguang& He, Zhiyi. 2020. Mir-141-3p Regulates Apoptosis and Mitochondrial Membrane Potential via Targeting Sirtuin1 in a 1-Methyl-4-Phenylpyridinium in vitro Model of Parkinson’s Disease. BioMed Research International،Vol. 2020, no. 2020, pp.1-14.
https://search.emarefa.net/detail/BIM-1136669
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Zheng, Yumin…[et al.]. Mir-141-3p Regulates Apoptosis and Mitochondrial Membrane Potential via Targeting Sirtuin1 in a 1-Methyl-4-Phenylpyridinium in vitro Model of Parkinson’s Disease. BioMed Research International No. 2020 (2020), pp.1-14.
https://search.emarefa.net/detail/BIM-1136669
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Zheng, Yumin& Dong, Li& Liu, Na& Luo, Xiaoguang& He, Zhiyi. Mir-141-3p Regulates Apoptosis and Mitochondrial Membrane Potential via Targeting Sirtuin1 in a 1-Methyl-4-Phenylpyridinium in vitro Model of Parkinson’s Disease. BioMed Research International. 2020. Vol. 2020, no. 2020, pp.1-14.
https://search.emarefa.net/detail/BIM-1136669
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1136669
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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