IL‐4 induces apoptosis of endothelial cells through the caspase‐3‐dependent pathway

FEBS Letters

Hennig, Bernhard²  Kühn, Hartmut¹  Lee, Yong Woo³  Toborek, Michal³ 

[1] Humboldt University, Berlin, Germany;Department of Animal Sciences, University of Kentucky Medical Center, Lexington, KY 40536, USA;Department of Surgery, University of Kentucky Medical Center, 800 Rose Street, Lexington, KY 40536, USA

关键词: Interleukin-4;    Apoptosis;    Human endothelial cell;    Caspase-3;    Atherosclerosis;    CHX;    cycloheximide;    HUVEC;    human umbilical vein endothelial cells;    IL-1β;    interleukin-1β;    IL-4;    interleukin-4;    TNF-α;    tumor necrosis factor-α;    VCAM-1;    vascular cell adhesion molecule-1;    zVAD-fmk;    z-Val-Ala-Asp-fluoromethylketone;   

DOI  :  10.1016/S0014-5793(00)02208-0

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The present study was designed to investigate the hypothesis that interleukin-4 (IL-4) can induce apoptosis of human endothelial cells and to study regulatory pathways of this process. Indeed, DNA ladder assay and flow cytometry study showed that IL-4 can induce apoptosis of endothelial cells in a time- and dose-dependent manner. In addition, IL-4 markedly increased activity of caspase-3, and inhibition of this enzyme suppressed IL-4-induced apoptosis in a dose-dependent manner. These results provide the first evidence that IL-4 can induce apoptosis of human endothelial cells. In addition, the data indicate that the caspase-3-dependent pathway is critically involved in this process.

【 授权许可】

Unknown