ArticleJournal of neural transmission (Vienna, Austria : 1996)2013
Rasagiline and selegiline, inhibitors of type B monoamine oxidase, induce type A monoamine oxidase in human SH-SY5Y cells.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Case Report: A possible novel adult-onset, progressive MAO-A hypofunction.Frontiers in neuroscience · 2026Article
- Deploying the drug repurposing approach for the identification of selective monoamine oxidase-B inhibitors against neurological disabilities: an in Silico and in vitro approach.Journal of computer-aided molecular design · 2025Article
- Type A monoamine oxidase; its unique role in mood, behavior and neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Exploring the 1-(4-Nitrophenyl)-3-arylprop-2-en-1-one Scaffold for the Selective Inhibition of Monoamine Oxidase B.ACS medicinal chemistry letters · 2024Article
- Latest advances in dual inhibitors of acetylcholinesterase and monoamine oxidase B against Alzheimer's disease.Journal of enzyme inhibition and medicinal chemistry · 2023Review
- Rasagiline and selegiline modulate mitochondrial homeostasis, intervene apoptosis system and mitigate α-synuclein cytotoxicity in disease-modifying therapy for Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Type A and B monoamine oxidases distinctly modulate signal transduction pathway and gene expression to regulate brain function and survival of neurons.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Neuroprotective effects of selegiline on rat neural stem cells treated with hydrogen peroxide.Biomedical reports · 2018Article
- Type A monoamine oxidase and serotonin are coordinately involved in depressive disorders: from neurotransmitter imbalance to impaired neurogenesis.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Type B and A monoamine oxidase and their inhibitors regulate the gene expression of Bcl-2 and neurotrophic factors in human glioblastoma U118MG cells: different signal pathways for neuroprotection by selegiline and rasagiline.Journal of neural transmission (Vienna, Austria : 1996) · 2017Article
- Aberrant CpG Methylation Mediates Abnormal Transcription of MAO-A Induced by Acute and Chronic L-3,4-Dihydroxyphenylalanine Administration in SH-SY5Y Neuronal Cells.Neurotoxicity research · 2017Article
- Neurotrophic and neuroprotective effects of oxyntomodulin in neuronal cells and a rat model of stroke.Experimental neurology · 2017Article
- Effects of Monoamine Oxidase Inhibition on the Reinforcing Properties of Low-Dose Nicotine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Modulation of monoamine oxidase (MAO) expression in neuropsychiatric disorders: genetic and environmental factors involved in type A MAO expression.Journal of neural transmission (Vienna, Austria : 1996) · 2016Review
- Cellular uptake of quercetin and luteolin and their effects on monoamine oxidase-A in human neuroblastoma SH-SY5Y cells.Toxicology reports · 2014Article
- Rasagiline prevents apoptosis induced by PK11195, a ligand of the outer membrane translocator protein (18 kDa), in SH-SY5Y cells through suppression of cytochrome c release from mitochondria.Journal of neural transmission (Vienna, Austria : 1996) · 2013Article
- Quantum-chemical approach to determining the high potency of clorgyline as an irreversible acetylenic monoamine oxidase inhibitor.Journal of neural transmission (Vienna, Austria : 1996) · 2013Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type B monoamine oxidase (MAO-B) is proposed to be involved in the pathogenesis of neurodegenerative disorders, such as Parkinson's disease, through oxidative stress and synthesis of neurotoxins. MAO-B inhibitors, rasagiline and selegiline [(-)deprenyl], protect neuronal cells by direct intervention in mitochondrial death signaling and induction of pro-survival Bcl-2 and neurotrophic factors. Recently, type A MAO (MAO-A) was found to mediate the induction of anti-apoptotic Bcl-2 by rasagiline, whereas MAO-A increases in neuronal death and also serves as a target of neurotoxins. These controversial results suggest that MAO-A may play a decisive role in neuronal survival and death. This paper reports that rasagiline and selegiline increased the mRNA, protein and catalytic activity of MAO-A in SH-SY5Y cells. Silencing MAO-A expression with small interfering (si)RNA suppressed rasagiline-dependent MAO-A expression, but MAO-B overexpression in SH-SY5Y cells did not affect, suggesting that MAO-A, not MAO-B, might be associated with MAO-A upregulation. Rasagiline reduced R1, a MAO-A specific repressor, but selegiline did not. Mithramycin-A, an inhibitor of Sp1 binding, and actinomycin-D, a transcriptional inhibitor, reduced the rasagiline-dependent upregulation of MAO-A mRNA, indicating that rasagiline induced MAO-A transcriptionally through R1-Sp1 pathway, whereas selegiline by another non-defined pathway. These results are discussed in relation to the role of MAO-A and these MAO-B inhibitors in neuronal death and neuroprotection.
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