NDLI: 15-Deoxy-$^{Δ12,14}$-prostaglandin J$_{2}$ (15d-PGJ$_{2}$) Induces Cell Death Through Caspase-independent Mechanism in A172 Human Glioma Cells

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15-Deoxy-$^{Δ12,14}$-prostaglandin J$_{2}$ (15d-PGJ$_{2}$) Induces Cell Death Through Caspase-independent Mechanism in A172 Human Glioma Cells

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15-Deoxy-$^{Δ12,14}$-prostaglandin J$_{2}$ (15d-PGJ$_{2}$) Induces Cell Death Through Caspase-independent Mechanism in A172 Human Glioma Cells

Content Provider	Springer Nature Link
Author	Cho, W. H. Choi, C. H. Park, J. Y. Kang, S. K. Kim, Y. K.
Copyright Year	2006
Abstract	15-Deoxy-$^{Δ12,14}$-prostaglandin J$_{2}$ (15d-PGJ$_{2}$) is a naturally occurring cyclopentenone metabolite of prostaglandin D$_{2}$ (PGD$_{2}$) and is known as a specific potent ligand for the peroxisome proliferators activator receptor-γ (PPARγ). 15d-PGJ$_{2}$ inhibits cell growth and induces apoptosis in a number of different cancer cells. However, the underlying mechanism by which 15d-PGJ$_{2}$ induces cell death remains to be defined. The present study was undertaken to determine the effect of 15d-PGJ$_{2}$ on cell death in A172 human glioma cells. 15d-PGJ$_{2}$ caused reactive oxygen species (ROS) generation. 15d-PGJ$_{2}$-induced ROS production and cell death were prevented by the antioxidant N-acetylcysteine. Activation of mitogen-activated protein kinases (MAPK) was not observed in cells treated with 15d-PGJ$_{2 }$and inhibitors of MAPK subfamilies also were not effective in preventing 15d-PGJ$_{2}$-induced cell death. 15d-PGJ$_{2}$ treatment caused mitochondrial dysfunction, as evidenced by depolarization of mitochondrial membrane potential. 15d-PGJ$_{2}$ induced caspase activation at 24 h of treatment, but the 15d-PGJ$_{2}$-induced cell death was not prevented by caspase inhibitors. The antiapoptotic protein XIAP levels and release of apoptosis inducing factor (AIF) into the cytosol were not altered by 15d-PGJ$_{2}$ treatment. Taken together, these findings indicate that 15d-PGJ$_{2}$ triggers cell death through a caspase-independent mechanism and ROS production and disruption of mitochondrial membrane potential play an important role in the 15d-PGJ$_{2}$-induced cell death in A172 human glioma cells.
Starting Page	1247
Ending Page	1254
Page Count	8
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	31
Issue Number	10
e-ISSN	15736903
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	2006-09-28
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	15d-PGJ$_{2}$ Caspase-independent apoptosis Mitochondrial depolarization Reactive oxygen species Human A172 glioma cells Neurology Biochemistry Neurosciences
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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