Expression of heme oxygenase-1 protects endothelial cells from irradiation-induced apoptosis

被引：20

作者：

Ewing, P

Wilke, A

Eissner, G

Holler, E

Andreesen, R

Gerbitz, A

机构：

[1] Univ Regensburg, Dept Hematol Oncol, D-93053 Regensburg, Germany

[2] GSF, Clin Cooperat Grp, Munich, Germany

[3] Univ Munich, Dept Hematol Oncol, Munich, Germany

来源：

ENDOTHELIUM-JOURNAL OF ENDOTHELIAL CELL RESEARCH | 2005年 / 12卷 / 03期

关键词：

apoptosis; endothelial; heme oxygenase-1; irradiation; protoporphyrine;

D O I：

10.1080/10623320500189814

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 [细胞生物学]; 090102 [作物遗传育种];

摘要：

A common side effect of therapeutic use of ionizing irradiation is endothelial cell damage resulting in a variety of clinical complications. Thus, preservation of endothelial function after irradiation could potentially limit toxicity. Using the murine endothelioma cell line bEnd2 we show here that induction of heme oxygenase-1 (HO-1) by cobalt protoporphyrine IX (CoPP) inhibits irradiation-induced apoptosis. In contrast, HO-1 induction by tin protoporphyrine IX (SnPP), a HO-1 inhibitor, does not affect survival after irradiation. The protective effects of CoPP could be partially reversed by blockade of HO-1 function with SnPP after induction by CoPP. Vice versa, blockade of HO-1 function by SnPP was reversible using CoPP. Treatment with CoPP inhibited cytochrome c release induced by irradiation. These results demonstrate that HO-1 induction and activation prior to irradiation inhibits endothelial apoptosis and might be used for possible cell protection in vivo.

引用

页码：113 / 119

页数：7

共 33 条

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p38 mitogen-activated protein kinase regulates a novel, caspase-independent pathway for the mitochondrial cytochrome c release in ultraviolet B radiation-induced apoptosis [J].