Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation.
10.4062/biomolther.2014.115
- Author:
Hong Joo SEO
1
;
Sang Joon CHOI
;
Jung Hee LEE
Author Information
1. Department of Thoracic and Cardiovascular Surgery, Chosun University Hospital, Gwangju 501-759, Republic of Korea.
- Publication Type:Original Article
- Keywords:
Paraquat;
NIH3T3 cells;
ERK1/2;
Apoptosis;
Cytochrome C;
MAPK
- MeSH:
Apoptosis*;
Cytochromes c*;
Negotiating;
Paraquat*;
Protein Kinases;
Reactive Oxygen Species
- From:Biomolecules & Therapeutics
2014;22(6):503-509
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
