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Differential effect of platelet activating factor on 1-methyl-4-phenylpyridinium-induced cell death through regulation of apoptosis-related protein activation.
Neurochem Int. 2010 May-Jun; 56(6-7):819-28.NI

Abstract

Platelet activating factor (PAF) has been suggested to play a critical role in the pathogenesis of neurological disorders. We assessed the effect of PAF against the toxicity of 1-methyl-4-phenylpyridinium (MPP(+)), a parkinsonian toxin, in relation to apoptotic process. PAF exhibited differential effect against the MPP(+) toxicity in differentiated PC12 cells depending on concentration. Treatment with 0.75 microM PAF significantly attenuated the MPP(+)-induced increase in Bax levels, decrease in Bid and Bcl-2 levels, and mitochondrial membrane potential loss that lead to the release of cytochrome c and subsequent caspase-3 activation. The inhibitory effect of PAF was not associated with nuclear factor-kappaB activation. In contrast, PAF at the concentrations greater than 2.5 microM exhibited a toxicity and additive effect on the MPP(+) toxicity. The results show that PAF at low concentrations, which does not induce a significant toxicity, may prevent the MPP(+) toxicity by suppressing the apoptosis-related protein activation and mitochondrial membrane permeability change that lead to the cytochrome c release and caspase-3 activation. The preventive effect seems to be associated with the inhibitory effect on the formation of reactive oxygen species and depletion of GSH. In contrast, PAF at higher concentrations may exhibit an additive toxic effect against the MPP(+) toxicity by increasing apoptosis-related protein activation.

Authors+Show Affiliations

Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, South Korea.No affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

20304020

Citation

Ha, Sang Won, and Chung Soo Lee. "Differential Effect of Platelet Activating Factor On 1-methyl-4-phenylpyridinium-induced Cell Death Through Regulation of Apoptosis-related Protein Activation." Neurochemistry International, vol. 56, no. 6-7, 2010, pp. 819-28.
Ha SW, Lee CS. Differential effect of platelet activating factor on 1-methyl-4-phenylpyridinium-induced cell death through regulation of apoptosis-related protein activation. Neurochem Int. 2010;56(6-7):819-28.
Ha, S. W., & Lee, C. S. (2010). Differential effect of platelet activating factor on 1-methyl-4-phenylpyridinium-induced cell death through regulation of apoptosis-related protein activation. Neurochemistry International, 56(6-7), 819-28. https://doi.org/10.1016/j.neuint.2010.03.006
Ha SW, Lee CS. Differential Effect of Platelet Activating Factor On 1-methyl-4-phenylpyridinium-induced Cell Death Through Regulation of Apoptosis-related Protein Activation. Neurochem Int. 2010 May-Jun;56(6-7):819-28. PubMed PMID: 20304020.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Differential effect of platelet activating factor on 1-methyl-4-phenylpyridinium-induced cell death through regulation of apoptosis-related protein activation. AU - Ha,Sang Won, AU - Lee,Chung Soo, Y1 - 2010/03/19/ PY - 2009/11/11/received PY - 2010/03/10/revised PY - 2010/03/12/accepted PY - 2010/3/23/entrez PY - 2010/3/23/pubmed PY - 2010/7/30/medline SP - 819 EP - 28 JF - Neurochemistry international JO - Neurochem Int VL - 56 IS - 6-7 N2 - Platelet activating factor (PAF) has been suggested to play a critical role in the pathogenesis of neurological disorders. We assessed the effect of PAF against the toxicity of 1-methyl-4-phenylpyridinium (MPP(+)), a parkinsonian toxin, in relation to apoptotic process. PAF exhibited differential effect against the MPP(+) toxicity in differentiated PC12 cells depending on concentration. Treatment with 0.75 microM PAF significantly attenuated the MPP(+)-induced increase in Bax levels, decrease in Bid and Bcl-2 levels, and mitochondrial membrane potential loss that lead to the release of cytochrome c and subsequent caspase-3 activation. The inhibitory effect of PAF was not associated with nuclear factor-kappaB activation. In contrast, PAF at the concentrations greater than 2.5 microM exhibited a toxicity and additive effect on the MPP(+) toxicity. The results show that PAF at low concentrations, which does not induce a significant toxicity, may prevent the MPP(+) toxicity by suppressing the apoptosis-related protein activation and mitochondrial membrane permeability change that lead to the cytochrome c release and caspase-3 activation. The preventive effect seems to be associated with the inhibitory effect on the formation of reactive oxygen species and depletion of GSH. In contrast, PAF at higher concentrations may exhibit an additive toxic effect against the MPP(+) toxicity by increasing apoptosis-related protein activation. SN - 1872-9754 UR - https://www.unboundmedicine.com/medline/citation/20304020/Differential_effect_of_platelet_activating_factor_on_1_methyl_4_phenylpyridinium_induced_cell_death_through_regulation_of_apoptosis_related_protein_activation_ DB - PRIME DP - Unbound Medicine ER -