ArticleJournal of neural transmission (Vienna, Austria : 1996)2017
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.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Repurposing neurological drugs for brain cancer therapeutics: A systematic approach to identify charged molecules for affinity-based local drug delivery systems.International journal of pharmaceutics · 2025Pooled it
- In-depth analysis of data from the RAS-ALS study reveals new insights in rasagiline treatment for amyotrophic lateral sclerosis.European journal of neurology · 2024Trial
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- Protective Effect of Selegiline (R-deprenyl) in Aminoglycoside-Induced Hearing Loss.Neurochemical research · 2025Article
- Generation and validation of a novel multitarget small molecule in glioblastoma.Cell death & disease · 2025Article
- Type A monoamine oxidase; its unique role in mood, behavior and neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Type-B monoamine oxidase inhibitors in neurological diseases: clinical applications based on preclinical findings.Neural regeneration research · 2024Review
- Inhibition of Enzymes Involved in Neurodegenerative Disorders and AMolecules (Basel, Switzerland) · 2023Article
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- Neuroprotective Function of Rasagiline and Selegiline, Inhibitors of Type B Monoamine Oxidase, and Role of Monoamine Oxidases in Synucleinopathies.International journal of molecular sciences · 2022Review
- Neuroprotective effect of L-deprenyl on the expression level of the Mst1 gene and inhibition of apoptosis in rat-model spinal cord injury.Iranian journal of basic medical sciences · 2022Article
- Evaluation of the combined activity of benzimidazole arylhydrazones as new anti-Parkinsonian agents: monoamine oxidase-B inhibition, neuroprotection and oxidative stress modulation.Neural regeneration research · 2021Article
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- Natural Products for Neurodegeneration: Regulating Neurotrophic Signals.Oxidative medicine and cellular longevity · 2021Review
- Parameters for Irreversible Inactivation of Monoamine Oxidase.Molecules (Basel, Switzerland) · 2020Article
- The Antiproliferative Effects of Flavonoid MAO Inhibitors on Prostate Cancer Cells.Molecules (Basel, Switzerland) · 2020Article
- 6-Hydroxydopamine: a far from simple neurotoxin.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- 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
- Early Life Stress Induced DNA Methylation of Monoamine Oxidases Leads to Depressive-Like Behavior.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type B monoamine oxidase (MAO-B) in glial cells has been considered to be associated with neuronal death in Parkinson's disease. MAO-B inhibitors, rasagiline and selegiline [(-)deprenyl], protect neurons in animal and cellular models of neurodegeneration. However, the role of MAO-B itself in the regulation of cell death processing remains elusive, whereas type A MAO (MAO-A) mediates the induction of anti-apoptotic Bcl-2 genes by rasagiline and selegiline. In this paper, the involvement of MAOs in the induction of neuroprotective genes by MAO inhibitors was investigated in human glioblastoma U118MG cells expressing mainly MAO-B. Selegiline significantly increased Mao-B, which was suppressed by Mao-A knockdown with short interfering (si)RNA, whereas rasagiline less markedly increased Mao-B, which was not affected by Mao-A knockdown. Mao-A mRNA was also markedly increased by rasagiline and selegiline, and Mao-B knockdown significantly enhanced the induction by selegiline, but not by rasagiline. Mao-B knockdown also significantly increased mRNA levels of Bcl-2, brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). Selegiline synergistically enhanced the expression of these genes in Mao-B knockdown cells, but Mao-A knockdown suppressed the increase. Rasagiline increased BDNF and GDNF, which Mao-B and Mao-A knockdown inhibited. These results show that MAO-B might function as a repressor and MAO-A as a mediator in the constitutional expression of pro-survival genes, and that MAO-B and MAO-A might regulate different signal pathways for rasagiline and selegiline to induce neuroprotective genes. The novel role of glial MAOs in the regulation of gene expression is discussed.
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