Limits...
Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation.

Seo HJ, Choi SJ, Lee JH - Biomol Ther (Seoul) (2014)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic and Cardiovascular Surgery, Chosun University School of Medicine, Gwangju 501-759, Republic of Korea.

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.

No MeSH data available.


Related in: MedlinePlus

Induction of apoptosis by paraquat in NIH3T3 cells. (A) NIH3T3 cells were treated with paraquat at final concentration indicated for 24 h. Cells were then stained with propidium iodide and apoptosis examined by flow cytometry. Each column shows the mean ± S.D. of triplicate experiments. * indicates a response that is significantly different from the control group as determined by two-tailed t test at p<0.05. (B) Cells were treated with different dose of paraquat for 24 h and DNA fragmentation was analyzed by 1.5% agarose gel electrophoresis. DNA bands were visualized by staining with ethidium bromide. (C) The chemical structure of paraquat.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4256029&req=5

f1-bt-22-503: Induction of apoptosis by paraquat in NIH3T3 cells. (A) NIH3T3 cells were treated with paraquat at final concentration indicated for 24 h. Cells were then stained with propidium iodide and apoptosis examined by flow cytometry. Each column shows the mean ± S.D. of triplicate experiments. * indicates a response that is significantly different from the control group as determined by two-tailed t test at p<0.05. (B) Cells were treated with different dose of paraquat for 24 h and DNA fragmentation was analyzed by 1.5% agarose gel electrophoresis. DNA bands were visualized by staining with ethidium bromide. (C) The chemical structure of paraquat.

Mentions: Accumulation evidences indicate that paraquat lead to cell death by the induction of apoptosis (Han et al., 2014; Wang et al., 2014c). Although several prior studies have investigated the mechanism of paraquat-induced apoptosis, however, it is not fully understood. In the present study, we therefore attempted to investigate the mechanism of paraquat-induced apoptosis using NIH3T3 cells. After exposure to 0.1, 0.25, 0.5, or 1 mM paraquat, sub-G1 DNA content and DNA fragmentation were evaluated in NIH3T3 cells. Fig. 1A showed that paraquat caused apoptosis of NIH3T3 cells in a dose-dependent manner, with a concentration of 1 mM paraquat resulting in death of greater than 80% of the cell population by 24 h of treatment. The intensity of paraquat-induced DNA ladders increased with increasing dose of paraquat in NIH3T3 cells (Fig. 1B). These data indicate that paraquat is able to induce apoptosis in a dose-dependent manner in NIH3T3 cells.


Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation.

Seo HJ, Choi SJ, Lee JH - Biomol Ther (Seoul) (2014)

Induction of apoptosis by paraquat in NIH3T3 cells. (A) NIH3T3 cells were treated with paraquat at final concentration indicated for 24 h. Cells were then stained with propidium iodide and apoptosis examined by flow cytometry. Each column shows the mean ± S.D. of triplicate experiments. * indicates a response that is significantly different from the control group as determined by two-tailed t test at p<0.05. (B) Cells were treated with different dose of paraquat for 24 h and DNA fragmentation was analyzed by 1.5% agarose gel electrophoresis. DNA bands were visualized by staining with ethidium bromide. (C) The chemical structure of paraquat.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4256029&req=5

f1-bt-22-503: Induction of apoptosis by paraquat in NIH3T3 cells. (A) NIH3T3 cells were treated with paraquat at final concentration indicated for 24 h. Cells were then stained with propidium iodide and apoptosis examined by flow cytometry. Each column shows the mean ± S.D. of triplicate experiments. * indicates a response that is significantly different from the control group as determined by two-tailed t test at p<0.05. (B) Cells were treated with different dose of paraquat for 24 h and DNA fragmentation was analyzed by 1.5% agarose gel electrophoresis. DNA bands were visualized by staining with ethidium bromide. (C) The chemical structure of paraquat.
Mentions: Accumulation evidences indicate that paraquat lead to cell death by the induction of apoptosis (Han et al., 2014; Wang et al., 2014c). Although several prior studies have investigated the mechanism of paraquat-induced apoptosis, however, it is not fully understood. In the present study, we therefore attempted to investigate the mechanism of paraquat-induced apoptosis using NIH3T3 cells. After exposure to 0.1, 0.25, 0.5, or 1 mM paraquat, sub-G1 DNA content and DNA fragmentation were evaluated in NIH3T3 cells. Fig. 1A showed that paraquat caused apoptosis of NIH3T3 cells in a dose-dependent manner, with a concentration of 1 mM paraquat resulting in death of greater than 80% of the cell population by 24 h of treatment. The intensity of paraquat-induced DNA ladders increased with increasing dose of paraquat in NIH3T3 cells (Fig. 1B). These data indicate that paraquat is able to induce apoptosis in a dose-dependent manner in NIH3T3 cells.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic and Cardiovascular Surgery, Chosun University School of Medicine, Gwangju 501-759, Republic of Korea.

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.

No MeSH data available.


Related in: MedlinePlus