Caspase-3-dependent apoptosis in vascular smooth muscle cell by proteasome inhibition

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Title
Caspase-3-dependent apoptosis in vascular smooth muscle cell by proteasome inhibition
Author(s)
S C Kim; Mun Chual RhoHyun Sun Lee; Young Kook Kim; Koanhoi Kim
Bibliographic Citation
Journal of Cardiovascular Pharmacology, vol. 42, no. 4, pp. 554-560
Publication Year
2003
Abstract
The effects of a number of substances on neointima formation following angioplasty have been investigated in animal models. It was suggested that delivering of proteasome inhibitor to the site of vascular injury would be a potential therapeutic approach in prevention of vascular restenosis. But the mechanisms underlying biologic activities of proteasome inhibition in vascular smooth muscle cells (VSMCs) are largely unknown. We have investigated effects of proteasome inhibition on VSMCs using proteasome inhibitor MG115. MG115 induced apoptotic death in VSMCs as determined by viability, morphology, and DNA fragmentation. Proteasome inhibition was accompanied by up-regulation of p53, p21, and p27. In contrast, there were no appreciable alterations in the levels of Bcl-2 and Bax. Proteasome inhibition was followed by activation of caspase-3 but not of -8. The induction of apoptosis was suppressed by treatment with a selective inhibitor of the caspase-3 family, z-DEVD-fmk but not by N G-monomethyl-L-arginine. These results indicate that proteasome inhibition induces apoptosis in VSMCs by activation of caspase-3.
Keyword
ApoptosisP53ProteasomeRestenosisSmooth muscle cell
ISSN
0160-2446
Publisher
Kluwer
DOI
http://dx.doi.org/10.1097/00005344-200310000-00014
Type
Article
Appears in Collections:
Jeonbuk Branch Institute > Immunoregulatory materials Research Center > 1. Journal Articles
Ochang Branch Institute > Natural Medicine Research Center > 1. Journal Articles
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