MG132, a proteasome inhibitor, induced death of calf pulmonary artery endothelial cells via caspase-dependent apoptosis and GSH depletion.

Abstract:

:MG132, a proteasome inhibitor, has been shown to induce apoptotic cell death through formation of reactive oxygen species (ROS). Here, we evaluated the effects of MG132 on the growth of endothelial cells, especially calf pulmonary artery endothelial cells (CPAECs). MG132 dose-dependently inhibited the growth of CPAECSs and human umbilical vein endothelial cells (HUVECs) at 24 hours. MG132 also induced apoptosis in both cell lines, which was accompanied by the loss of mitochondrial membrane potential. All the tested caspase inhibitors (pan-caspase, caspase-3, -8 and -9 inhibitor) significantly rescued CPAECs from MG132-induced cell death. MG132 increased ROS level and GSH depleted cell numbers of CPAECs. None of the caspase inhibitors reduced ROS level in MG132-treated CPAECs but did reduce apoptosis in these cells. In conclusion, MG132 inhibited the growth of endothelial cells, especially CPAECs via caspase-dependent apoptosis. MG132-induced CPAEC death was related to GSH depletion rather than a change in ROS level.

journal_name

Anticancer Res

journal_title

Anticancer research

authors

Han YH,Moon HJ,You BR,Yang YM,Kim SZ,Kim SH,Park WH

subject

Has Abstract

pub_date

2010-03-01 00:00:00

pages

879-85

issue

3

eissn

0250-7005

issn

1791-7530

pii

30/3/879

journal_volume

30

pub_type

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