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Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation

Paraquat has been suggested to induce apoptosis by generation of reactive oxygen species (ROS). However, little is known about the mechanism of paraquat-induced apoptosis. Here, we demonstrate that extracellular signal-regulated protein kinase (ERK) is required for paraquat-induced apoptosis in NIH3...

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Detalles Bibliográficos
Autores principales: Seo, Hong Joo, Choi, Sang Joon, Lee, Jung-Hee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Applied Pharmacology 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4256029/
https://www.ncbi.nlm.nih.gov/pubmed/25489417
http://dx.doi.org/10.4062/biomolther.2014.115
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author Seo, Hong Joo
Choi, Sang Joon
Lee, Jung-Hee
author_facet Seo, Hong Joo
Choi, Sang Joon
Lee, Jung-Hee
author_sort Seo, Hong Joo
collection PubMed
description Paraquat has been suggested to induce apoptosis by generation of reactive oxygen species (ROS). However, little is known about the mechanism of paraquat-induced apoptosis. Here, we demonstrate that extracellular signal-regulated protein kinase (ERK) is required for paraquat-induced apoptosis in NIH3T3 cells. Paraquat treatment resulted in activation of ERK, and U0126, inhibitors of the MEK/ERK signaling pathway, prevented apoptosis. Moreover, paraquat-induced apoptosis was associated with cytochrome C release, which could be prevented by treatment with the MEK inhibitors. Taken together, our findings suggest that ERK activation plays an active role in mediating paraquat-induced apoptosis of NIH3T3 cells.
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spelling pubmed-42560292014-12-08 Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation Seo, Hong Joo Choi, Sang Joon Lee, Jung-Hee Biomol Ther (Seoul) Original Article Paraquat has been suggested to induce apoptosis by generation of reactive oxygen species (ROS). However, little is known about the mechanism of paraquat-induced apoptosis. Here, we demonstrate that extracellular signal-regulated protein kinase (ERK) is required for paraquat-induced apoptosis in NIH3T3 cells. Paraquat treatment resulted in activation of ERK, and U0126, inhibitors of the MEK/ERK signaling pathway, prevented apoptosis. Moreover, paraquat-induced apoptosis was associated with cytochrome C release, which could be prevented by treatment with the MEK inhibitors. Taken together, our findings suggest that ERK activation plays an active role in mediating paraquat-induced apoptosis of NIH3T3 cells. The Korean Society of Applied Pharmacology 2014-11 2014-11-30 /pmc/articles/PMC4256029/ /pubmed/25489417 http://dx.doi.org/10.4062/biomolther.2014.115 Text en Copyright ©2014, The Korean Society of Applied Pharmacology http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Seo, Hong Joo
Choi, Sang Joon
Lee, Jung-Hee
Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation
title Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation
title_full Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation
title_fullStr Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation
title_full_unstemmed Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation
title_short Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation
title_sort paraquat induces apoptosis through cytochrome c release and erk activation
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4256029/
https://www.ncbi.nlm.nih.gov/pubmed/25489417
http://dx.doi.org/10.4062/biomolther.2014.115
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