Methylmercury can induce Parkinson's-like neurotoxicity similar to 1-methyl-4- phenylpyridinium: a genomic and proteomic analysis on MN9D dopaminergic neuron cells.
Identifieur interne : 000648 ( Main/Curation ); précédent : 000647; suivant : 000649Methylmercury can induce Parkinson's-like neurotoxicity similar to 1-methyl-4- phenylpyridinium: a genomic and proteomic analysis on MN9D dopaminergic neuron cells.
Auteurs : Yueting Shao [Canada] ; Daniel Figeys ; Zhibin Ning ; Ryan Mailloux ; Hing Man ChanSource :
- The Journal of toxicological sciences [ 1880-3989 ] ; 2015.
English descriptors
- KwdEn :
- 1-Methyl-4-phenylpyridinium (toxicity), Cells, Cultured, Dopamine (metabolism), Dopamine (physiology), Dopaminergic Neurons (metabolism), Energy Metabolism (genetics), Genome (drug effects), Genomics, Humans, Methylmercury Compounds (toxicity), Neurotoxicity Syndromes (etiology), Oxidative Phosphorylation, Parkinson Disease, Secondary (chemically induced), Proteasome Endopeptidase Complex, Proteome (drug effects), Proteomics, Signal Transduction (drug effects), Tyrosine 3-Monooxygenase (metabolism), Ubiquitin-Conjugating Enzymes (metabolism).
- MESH :
- chemical , drug effects : Proteome.
- chemical , metabolism : Dopamine, Tyrosine 3-Monooxygenase, Ubiquitin-Conjugating Enzymes.
- chemical , physiology : Dopamine.
- chemical , toxicity : 1-Methyl-4-phenylpyridinium, Methylmercury Compounds.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Genome, Signal Transduction.
- etiology : Neurotoxicity Syndromes.
- genetics : Energy Metabolism.
- metabolism : Dopaminergic Neurons.
- Cells, Cultured, Genomics, Humans, Oxidative Phosphorylation, Proteasome Endopeptidase Complex, Proteomics.
Abstract
Exposure to environmental chemicals has been implicated as a possible risk factor for the development of neurodegenerative diseases. Our previous study showed that methylmercury (MeHg) exposure can disrupt synthesis, uptake and metabolism of dopamine similar to 1-methyl-4-phenylpyridinium (MPP(+)). The objective of this study was to investigate the effects of MeHg exposure on gene and protein profiles in a dopaminergic MN9D cell line. MN9D cells were treated with MeHg (1-5 μM) and MPP(+) (10-40 μM) for 48 hr. Real-time PCR Parkinson's disease (PD) arrays and high-performance liquid chromatography/electrospray ionization tandem mass spectrometry (HPLC-ESI-MS/MS) were performed for the analysis. PD PCR array results showed that 19% genes were significantly changed in the 2.5 μM MeHg treated cells, and 39% genes were changed in the 5 μM MeHg treated cells. In comparison, MPP(+) treatment (40 µM) resulted in significant changes in 25% genes. A total of 15 common genes were altered by both MeHg and MPP(+), and dopaminergic signaling transduction was the most affected pathway. Proteomic analysis identified a total of 2496 proteins, of which 188, 233 and 395 proteins were differentially changed by 1 μM and 2.5 μM MeHg, and MPP(+) respectively. A total of 61 common proteins were changed by both MeHg and MPP(+) treatment. The changed proteins were mainly involved in energetic generation-related metabolism pathway (propanoate metabolism, pyruvate metabolism and fatty acid metabolism), oxidative phosphorylation, proteasome, PD and other neurodegenerative disorders. A total of 7 genes/proteins including Ube2l3 (Ubiquitin-conjugating enzyme E2 L3) and Th (Tyrosine 3-monooxygenase) were changed in both genomic and proteomic analysis. These results suggest that MeHg and MPP(+) share many similar signaling pathways leading to the pathogenesis of PD and other neurodegenerative diseases.
DOI: 10.2131/jts.40.817
PubMed: 26558463
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first="Zhibin" last="Ning">Zhibin Ning</name></author><author><name sortKey="Mailloux, Ryan" sort="Mailloux, Ryan" uniqKey="Mailloux R" first="Ryan" last="Mailloux">Ryan Mailloux</name></author><author><name sortKey="Chan, Hing Man" sort="Chan, Hing Man" uniqKey="Chan H" first="Hing Man" last="Chan">Hing Man Chan</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:26558463</idno><idno type="pmid">26558463</idno><idno type="doi">10.2131/jts.40.817</idno><idno type="wicri:Area/PubMed/Corpus">000363</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000363</idno><idno type="wicri:Area/PubMed/Curation">000363</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000363</idno><idno type="wicri:Area/PubMed/Checkpoint">000363</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000363</idno><idno 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Columbia</wicri:noRegion></affiliation></author><author><name sortKey="Figeys, Daniel" sort="Figeys, Daniel" uniqKey="Figeys D" first="Daniel" last="Figeys">Daniel Figeys</name></author><author><name sortKey="Ning, Zhibin" sort="Ning, Zhibin" uniqKey="Ning Z" first="Zhibin" last="Ning">Zhibin Ning</name></author><author><name sortKey="Mailloux, Ryan" sort="Mailloux, Ryan" uniqKey="Mailloux R" first="Ryan" last="Mailloux">Ryan Mailloux</name></author><author><name sortKey="Chan, Hing Man" sort="Chan, Hing Man" uniqKey="Chan H" first="Hing Man" last="Chan">Hing Man Chan</name></author></analytic><series><title level="j">The Journal of toxicological sciences</title><idno type="eISSN">1880-3989</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenylpyridinium (toxicity)</term><term>Cells, Cultured</term><term>Dopamine 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type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>1-Methyl-4-phenylpyridinium</term><term>Methylmercury Compounds</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Genome</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Neurotoxicity Syndromes</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Energy Metabolism</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dopaminergic Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cells, Cultured</term><term>Genomics</term><term>Humans</term><term>Oxidative Phosphorylation</term><term>Proteasome Endopeptidase Complex</term><term>Proteomics</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Exposure to environmental chemicals has been implicated as a possible risk factor for the development of neurodegenerative diseases. Our previous study showed that methylmercury (MeHg) exposure can disrupt synthesis, uptake and metabolism of dopamine similar to 1-methyl-4-phenylpyridinium (MPP(+)). The objective of this study was to investigate the effects of MeHg exposure on gene and protein profiles in a dopaminergic MN9D cell line. MN9D cells were treated with MeHg (1-5 μM) and MPP(+) (10-40 μM) for 48 hr. Real-time PCR Parkinson's disease (PD) arrays and high-performance liquid chromatography/electrospray ionization tandem mass spectrometry (HPLC-ESI-MS/MS) were performed for the analysis. PD PCR array results showed that 19% genes were significantly changed in the 2.5 μM MeHg treated cells, and 39% genes were changed in the 5 μM MeHg treated cells. In comparison, MPP(+) treatment (40 µM) resulted in significant changes in 25% genes. A total of 15 common genes were altered by both MeHg and MPP(+), and dopaminergic signaling transduction was the most affected pathway. Proteomic analysis identified a total of 2496 proteins, of which 188, 233 and 395 proteins were differentially changed by 1 μM and 2.5 μM MeHg, and MPP(+) respectively. A total of 61 common proteins were changed by both MeHg and MPP(+) treatment. The changed proteins were mainly involved in energetic generation-related metabolism pathway (propanoate metabolism, pyruvate metabolism and fatty acid metabolism), oxidative phosphorylation, proteasome, PD and other neurodegenerative disorders. A total of 7 genes/proteins including Ube2l3 (Ubiquitin-conjugating enzyme E2 L3) and Th (Tyrosine 3-monooxygenase) were changed in both genomic and proteomic analysis. These results suggest that MeHg and MPP(+) share many similar signaling pathways leading to the pathogenesis of PD and other neurodegenerative diseases.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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