Biomaterial Database

miR-124-3p attenuates MPP+-induced neuronal injury by targeting STAT3 in SH-SY5Y cells. 2017

Lijiao Geng, and Wei Liu, and Yong Chen

1 Department of Rehabilitation Medicine, Huaihe Hospital of Henan University, Kaifeng 475000, China.

Ample evidence has demonstrated the involvement of microRNAs in Parkinson's disease pathogenesis. miR-124-3p was reported to be able to improve neural functional recovery. However, the underlying mechanism of miR-124-3p in Parkinson's disease progression was not well established. This study was designed to investigate the role of miR-124-3p in methyl phenyl pyridinium iodide (MPP)+-induced SH-SY5Y cells, an in vitro Parkinson's disease model. It is observed that miR-124-3p expression was decreased, and STAT3 expression was increased in MPP+-induced SH-SY5Y cells. miR-124-3p overexpression attenuated MPP+-induced neuronal injury, displayed as increased cell viability and superoxide dismutase activities, as well as reduced cell apoptosis, Caspase-3 activity, lactate dehydrogenase activity, inflammatory factors TNF-α, and IL-1β levels and reactive oxygen species generation. Moreover, STAT3 was confirmed to be a miR-124-3p target. Restored STAT3 expression reversed miR-124-3p-induced neuroprotective effects against MPP+-mediated neuronal injury. These data demonstrated that miR-124-3p contributed to neuroprotective effects in MPP+-induced Parkinson's disease cell model by targeting STAT3. Impact statement PD affects millions of people in the world, causing uncontrolled tremors. MicroRNAs, a class of endogenous single-stranded non-coding transcript with approximately 22 nucleotides, could bind to the 3″ UTR of their targets. The functional action of miR-124-3p in PD was not fully elucidated. Our study found that ectopic expression miR-124-3p attenuated MPP+-induced injury in PD model in vitro by suppressing neurotoxicity, neuronal apoptosis, neuroinflammation, and oxidative stress. Moreover, we validated that miR-124-3p could bind to STAT3 mediating the neuroprotective effect of miR-124-3p. We believe this study will be interesting for readers of this area.

UI	MeSH Term	Description	Entries
D002470	Cell Survival	The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.	Cell Viability,Cell Viabilities,Survival, Cell,Viabilities, Cell,Viability, Cell
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D014409	Tumor Necrosis Factor-alpha	Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.	Cachectin,TNF-alpha,Tumor Necrosis Factor Ligand Superfamily Member 2,Cachectin-Tumor Necrosis Factor,TNF Superfamily, Member 2,TNFalpha,Tumor Necrosis Factor,Cachectin Tumor Necrosis Factor,Tumor Necrosis Factor alpha
D015655	1-Methyl-4-phenylpyridinium	An active neurotoxic metabolite of 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE. The compound reduces dopamine levels, inhibits the biosynthesis of catecholamines, depletes cardiac norepinephrine and inactivates tyrosine hydroxylase. These and other toxic effects lead to cessation of oxidative phosphorylation, ATP depletion, and cell death. The compound, which is related to PARAQUAT, has also been used as an herbicide.	Cyperquat,1-Methyl-4-phenylpyridine,1-Methyl-4-phenylpyridinium Chloride,1-Methyl-4-phenylpyridinium Ion,N-Methyl-4-phenylpyridine,N-Methyl-4-phenylpyridinium,1 Methyl 4 phenylpyridine,1 Methyl 4 phenylpyridinium,1 Methyl 4 phenylpyridinium Chloride,1 Methyl 4 phenylpyridinium Ion,N Methyl 4 phenylpyridine
D017209	Apoptosis	A regulated cell death mechanism characterized by distinctive morphologic changes in the nucleus and cytoplasm, including the endonucleolytic cleavage of genomic DNA, at regularly spaced, internucleosomal sites, i.e., DNA FRAGMENTATION. It is genetically programmed and serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.	Apoptosis, Extrinsic Pathway,Apoptosis, Intrinsic Pathway,Caspase-Dependent Apoptosis,Classic Apoptosis,Classical Apoptosis,Programmed Cell Death,Programmed Cell Death, Type I,Apoptoses, Extrinsic Pathway,Apoptoses, Intrinsic Pathway,Apoptosis, Caspase-Dependent,Apoptosis, Classic,Apoptosis, Classical,Caspase Dependent Apoptosis,Cell Death, Programmed,Classic Apoptoses,Extrinsic Pathway Apoptoses,Extrinsic Pathway Apoptosis,Intrinsic Pathway Apoptoses,Intrinsic Pathway Apoptosis
D017382	Reactive Oxygen Species	Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of SIGNAL TRANSDUCTION and GENE EXPRESSION, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.	Active Oxygen Species,Oxygen Radical,Oxygen Radicals,Pro-Oxidant,Reactive Oxygen Intermediates,Active Oxygen,Oxygen Species, Reactive,Pro-Oxidants,Oxygen, Active,Pro Oxidant,Pro Oxidants,Radical, Oxygen
D045744	Cell Line, Tumor	A cell line derived from cultured tumor cells.	Tumor Cell Line,Cell Lines, Tumor,Line, Tumor Cell,Lines, Tumor Cell,Tumor Cell Lines
D050796	STAT3 Transcription Factor	A signal transducer and activator of transcription that mediates cellular responses to INTERLEUKIN-6 family members. STAT3 is constitutively activated in a variety of TUMORS and is a major downstream transducer for the CYTOKINE RECEPTOR GP130.	APRF Transcription Factor,Acute-Phase Response Factor,IL6-Response Factor,LIF-Response Factor,STAT3 Protein,STAT3a Transcription Factor,STAT3b Transcription Factor,Signal Transducer and Activator of Transcription 3,Stat3alpha Transcription Factor,Stat3beta Transcription Factor,Acute Phase Response Factor,IL6 Response Factor,LIF Response Factor,Response Factor, Acute-Phase,Transcription Factor, APRF,Transcription Factor, STAT3,Transcription Factor, STAT3a,Transcription Factor, STAT3b,Transcription Factor, Stat3alpha,Transcription Factor, Stat3beta
D018384	Oxidative Stress	A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).	Anti-oxidative Stress,Antioxidative Stress,DNA Oxidative Damage,Nitro-Oxidative Stress,Oxidative Cleavage,Oxidative DNA Damage,Oxidative Damage,Oxidative Injury,Oxidative Nitrative Stress,Oxidative Stress Injury,Oxidative and Nitrosative Stress,Stress, Oxidative,Anti oxidative Stress,Anti-oxidative Stresses,Antioxidative Stresses,Cleavage, Oxidative,DNA Damage, Oxidative,DNA Oxidative Damages,Damage, DNA Oxidative,Damage, Oxidative,Damage, Oxidative DNA,Injury, Oxidative,Injury, Oxidative Stress,Nitrative Stress, Oxidative,Nitro Oxidative Stress,Nitro-Oxidative Stresses,Oxidative Cleavages,Oxidative DNA Damages,Oxidative Damage, DNA,Oxidative Damages,Oxidative Injuries,Oxidative Nitrative Stresses,Oxidative Stress Injuries,Oxidative Stresses,Stress Injury, Oxidative,Stress, Anti-oxidative,Stress, Antioxidative,Stress, Nitro-Oxidative,Stress, Oxidative Nitrative,Stresses, Nitro-Oxidative
D018696	Neuroprotective Agents	Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.	Neuroprotectant,Neuroprotective Agent,Neuroprotective Drug,Neuroprotectants,Neuroprotective Drugs,Neuroprotective Effect,Neuroprotective Effects,Agent, Neuroprotective,Agents, Neuroprotective,Drug, Neuroprotective,Drugs, Neuroprotective,Effect, Neuroprotective,Effects, Neuroprotective