|
KMID : 0378020070500050011
|
|
New Medical Journal
2007 Volume.50 No. 5 p.11 ~ p.18
|
|
|
15-Deoxy-Δ12,14-Prostaglandin J2 Induces Cell Death Through Reactive Oxygen Species-Dependent Mechanism in Osteoblastic Cells
|
|
Jung Soon-Hee
|
|
|
Abstract
|
|
|
|
The present study was carried out to examine the molecular mechanism of cell death induced by PPARγagonists in osteoblastic cells. The endogenous PPARγagonist 15- Deoxy-Δ12,14-prostaglandin J2 (15-d-PGJ2) resulted in cell death in a concentration-dependent manner. But the PPARαagonist ciprofibrate did not affect the cell death. 15-d-PGJ2 caused reactive oxygen species (ROS) generation and 15-d-PGJ2 -induced cell death was prevented by antioxidants, suggesting a critical role of ROS generation in 15-d-PGJ2 - induced cell death. 15-d-PGJ2 induced a loss of mitochondrial membrane potential and its effect was prevented by N-acetylcysteine. 15-d-PGJ2 induced caspase activation, which was prevented by N-acetylcysteine. 15-d-PGJ2 -induced cell death was prevented by the general caspase inhibitor z-DEVD-FMK. Taken together, these findings suggest that the ROS generation plays an active role in mediating 15-d-PGJ2 -induced cell death of osteoblasts and function upstream of a mitochondria-dependent mechanism. These data may provide a novel insight into potential therapeutic strategies for treatment of osteoporosis.
|
|
|
KEYWORD
|
|
|
Osteoblastic cells, 15-d-PGJ2, ROS, Cell death, Mouse
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|