The Role of Phospholipid Methylation in 1-Methyl-4-Phenyl-Pyridinium Ion (MPP +)-Induced Neurotoxicity in PC12 Cells

Excessive methylation has been proposed to be involved in the pathogenesis of Parkinson's disease (PD), via mechanisms that involve phospholipid methylation. Meanwhile, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was found to stimulate phospholipid methylation via the oxidized metabolit...

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Published inNeurotoxicology (Park Forest South) Vol. 26; no. 6; pp. 945 - 957
Main Authors Lee, Eun-Sook Y., Chen, Hongtao, Charlton, Clivel G., Soliman, Karam F.A.
Format Journal Article
LanguageEnglish
Published Orlando, FL Elsevier B.V 01.12.2005
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Abstract Excessive methylation has been proposed to be involved in the pathogenesis of Parkinson's disease (PD), via mechanisms that involve phospholipid methylation. Meanwhile, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was found to stimulate phospholipid methylation via the oxidized metabolite, 1-methyl-4-phenyl-pyridinium (MPP +), in the rat brain and liver tissues. In the present study, we investigated the effect of MPP + on phosphatidylethanolamine N-methyltransferases (PENMT) and the potential role of this pathway in MPP +-induced neurotoxicity using PC12 cells. The results obtained indicate that MPP + stimulated phosphatidylethanolamine (PTE) methylation to phosphatidylcholine (PTC) and correspondingly increased the formation of lysophosphatidylcholine (lyso-PTC). Moreover, the addition of S-adenosylmethionine (SAM) to the cell culture medium increases MPP +-induced cytotoxicity. The incubation of 1 mM MPP + and various concentrations of SAM (0–4 mM) decreased the viability of PC12 cells from 80% with MPP + alone to 38% viability with 4 mM SAM for 4 days incubation. The data also revealed that the addition of S-adenosylhomocysteine (SAH), a methylation inhibitor, offered significant protection against MPP +-induced cytotoxicity, indicating that methylation plays a role in MPP +-induced cytotoxicity. Interestingly, lyso-PTC showed similar actions to MPP + in causing many cytotoxic changes with at least 10 times higher potency. Lyso-PTC induced dopamine release and inhibited dopamine uptake in PC12 cells. Lyso-PTC also caused the inhibition of mitochondrial potential and increased the formation of reactive oxygen species in PC12 cells. These results indicate that phospholipid methylation pathway might be involved in MPP + neurotoxicity and lyso-PTC might play a role in MPP +-induced neurotoxicity.
AbstractList Excessive methylation has been proposed to be involved in the pathogenesis of Parkinson's disease (PD), via mechanisms that involve phospholipid methylation. Meanwhile, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was found to stimulate phospholipid methylation via the oxidized metabolite, 1-methyl-4-phenyl-pyridinium (MPP+), in the rat brain and liver tissues. In the present study, we investigated the effect of MPP+ on phosphatidylethanolamine N-methyltransferases (PENMT) and the potential role of this pathway in MPP(+)-induced neurotoxicity using PC12 cells. The results obtained indicate that MPP+ stimulated phosphatidylethanolamine (PTE) methylation to phosphatidylcholine (PTC) and correspondingly increased the formation of lysophosphatidylcholine (lyso-PTC). Moreover, the addition of S-adenosylmethionine (SAM) to the cell culture medium increases MPP(+)-induced cytotoxicity. The incubation of 1mM MPP+ and various concentrations of SAM (0-4 mM) decreased the viability of PC12 cells from 80% with MPP+ alone to 38% viability with 4 mM SAM for 4 days incubation. The data also revealed that the addition of S-adenosylhomocysteine (SAH), a methylation inhibitor, offered significant protection against MPP(+)-induced cytotoxicity, indicating that methylation plays a role in MPP(+)-induced cytotoxicity. Interestingly, lyso-PTC showed similar actions to MPP+ in causing many cytotoxic changes with at least 10 times higher potency. Lyso-PTC induced dopamine release and inhibited dopamine uptake in PC12 cells. Lyso-PTC also caused the inhibition of mitochondrial potential and increased the formation of reactive oxygen species in PC12 cells. These results indicate that phospholipid methylation pathway might be involved in MPP+ neurotoxicity and lyso-PTC might play a role in MPP(+)-induced neurotoxicity.
Excessive methylation has been proposed to be involved in the pathogenesis of Parkinson's disease (PD), via mechanisms that involve phospholipid methylation. Meanwhile, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was found to stimulate phospholipid methylation via the oxidized metabolite, 1-methyl-4-phenyl-pyridinium (MPP +), in the rat brain and liver tissues. In the present study, we investigated the effect of MPP + on phosphatidylethanolamine N-methyltransferases (PENMT) and the potential role of this pathway in MPP +-induced neurotoxicity using PC12 cells. The results obtained indicate that MPP + stimulated phosphatidylethanolamine (PTE) methylation to phosphatidylcholine (PTC) and correspondingly increased the formation of lysophosphatidylcholine (lyso-PTC). Moreover, the addition of S-adenosylmethionine (SAM) to the cell culture medium increases MPP +-induced cytotoxicity. The incubation of 1 mM MPP + and various concentrations of SAM (0–4 mM) decreased the viability of PC12 cells from 80% with MPP + alone to 38% viability with 4 mM SAM for 4 days incubation. The data also revealed that the addition of S-adenosylhomocysteine (SAH), a methylation inhibitor, offered significant protection against MPP +-induced cytotoxicity, indicating that methylation plays a role in MPP +-induced cytotoxicity. Interestingly, lyso-PTC showed similar actions to MPP + in causing many cytotoxic changes with at least 10 times higher potency. Lyso-PTC induced dopamine release and inhibited dopamine uptake in PC12 cells. Lyso-PTC also caused the inhibition of mitochondrial potential and increased the formation of reactive oxygen species in PC12 cells. These results indicate that phospholipid methylation pathway might be involved in MPP + neurotoxicity and lyso-PTC might play a role in MPP +-induced neurotoxicity.
Excessive methylation has been proposed to be involved in the pathogenesis of Parkinson's disease (PD), via mechanisms that involve phospholipid methylation. Meanwhile, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was found to stimulate phospholipid methylation via the oxidized metabolite, 1-methyl-4-phenyl-pyridinium (MPP+), in the rat brain and liver tissues. In the present study, we investigated the effect of MPP+ on phosphatidylethanolamine N-methyltransferases (PENMT) and the potential role of this pathway in MPP+-induced neurotoxicity using PC12 cells. The results obtained indicate that MPP+ stimulated phosphatidylethanolamine (PTE) methylation to phosphatidylcholine (PTC) and correspondingly increased the formation of lysophosphatidylcholine (lyso-PTC). Moreover, the addition of S-adenosylmethionine (SAM) to the cell culture medium increases MPP+-induced cytotoxicity. The incubation of 1mM MPP+ and various concentrations of SAM (0-4mM) decreased the viability of PC12 cells from 80% with MPP+ alone to 38% viability with 4mM SAM for 4 days incubation. The data also revealed that the addition of S-adenosylhomocysteine (SAH), a methylation inhibitor, offered significant protection against MPP+-induced cytotoxicity, indicating that methylation plays a role in MPP+-induced cytotoxicity. Interestingly, lyso-PTC showed similar actions to MPP+ in causing many cytotoxic changes with at least 10 times higher potency. Lyso-PTC induced dopamine release and inhibited dopamine uptake in PC12 cells. Lyso-PTC also caused the inhibition of mitochondrial potential and increased the formation of reactive oxygen species in PC12 cells. These results indicate that phospholipid methylation pathway might be involved in MPP+ neurotoxicity and lyso-PTC might play a role in MPP+-induced neurotoxicity.
Author Chen, Hongtao
Lee, Eun-Sook Y.
Charlton, Clivel G.
Soliman, Karam F.A.
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Issue 6
Keywords Phospholipid methylation
Parkinson's disease
MPP
PC12 cells
Lysophosphatidylcholine
S-Adenosylmethionine
Nervous system diseases
Adenosylmethionine
Toxicity
Parkinson disease
Phospholipid
Lipids
Cerebral disorder
Central nervous system disease
Degenerative disease
Methylation
Extrapyramidal syndrome
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Snippet Excessive methylation has been proposed to be involved in the pathogenesis of Parkinson's disease (PD), via mechanisms that involve phospholipid methylation....
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SubjectTerms 1-Methyl-4-phenylpyridinium
Animals
Biological and medical sciences
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Dopamine - metabolism
Lysophosphatidylcholine
Lysophosphatidylcholines - biosynthesis
Lysophosphatidylcholines - metabolism
Medical sciences
Methylation - drug effects
MPP
MPTP Poisoning - metabolism
Nervous system (semeiology, syndromes)
Nervous system as a whole
Neurology
Parkinson's disease
PC12 Cells
Phosphatidylcholines - biosynthesis
Phosphatidylethanolamine N-Methyltransferase - drug effects
Phosphatidylethanolamine N-Methyltransferase - metabolism
Phosphatidylethanolamines - metabolism
Phospholipid methylation
Phospholipids - metabolism
Rats
S-Adenosylhomocysteine - pharmacology
S-Adenosylmethionine
S-Adenosylmethionine - pharmacology
Toxicology
Title The Role of Phospholipid Methylation in 1-Methyl-4-Phenyl-Pyridinium Ion (MPP +)-Induced Neurotoxicity in PC12 Cells
URI https://dx.doi.org/10.1016/j.neuro.2005.04.005
https://www.ncbi.nlm.nih.gov/pubmed/15950286
https://search.proquest.com/docview/19723856
Volume 26
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