|
KMID : 0613820080180111513
|
|
Journal of Life Science
2008 Volume.18 No. 11 p.1513 ~ p.1520
|
|
|
4-Hydroxynonenal Induces Endothelial Apoptosis through Mitochondrial Depolarization
|
|
Kang Dae-Yeon
Lee Ji-Young
Kim Min-Sun
Kim Chul-Hong
Kim Hyung-Keun
Lee Sun-Mi
Kwon Young-Mi
Lee Jae-Won
Baik Hyung-Suk
Yu Byung-Pal
Chung Hae-Young
|
|
|
Abstract
|
|
|
|
The 4-Hydroxynonenal (HNE) affects vascular dysfunctions probably through the interruption of the cellular redox balance. To better understand vascular abnormalities resulting from the accumulation of HNE, we delineated mechanism by which mitochondrial apoptosis occurs in the YPEN-1 endothelial cells. HNE treatment led to the loss of mitochondrial membrane potential (δΨm), resulting in the release of cytochrome c. Data showed decreased Bcl-2 and increased Bax protein levels in HNE-treated cells. NAC, a reactive oxygen species (ROS) scavenger, and penicillamine, the peroxynitrite scavenger, blocked HNE-mediated ROS generation, thereby thwarting the cytochrome c release and apoptosis. The treatment of the cells with zVAD-fmk, a broad range caspase inhibitor did not suppress HNE-induced apoptosis, suggesting that the apoptosis might be the possibility of caspase-independent process. Our findings delineate the underlying mechanism of the HNE induced endothelial apoptosis by triggering depolarization of mitochondria membrane potential that can lead to the deterioration of vasculature homeostasis and subsequent vascular dysfunction with aging.
|
|
|
KEYWORD
|
|
|
4-Hydroxynonenal, apoptosis, mitochondrial membrane potential, caspase-3, cytochrome C release
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|