β-Lapachone, a Quinone Isolated from Tabebuia avellanedae, Induces Apoptosis in HepG2 Hepatoma Cell Line Through Induction of Bax and Activation of Caspase

2006 ◽  
Vol 9 (2) ◽  
pp. 161-168 ◽  
Author(s):  
Hyun Joo Woo ◽  
Kun-Young Park ◽  
Chung-Ho Rhu ◽  
Won Ho Lee ◽  
Byung Tae Choi ◽  
...  
Life Sciences ◽  
2010 ◽  
Vol 86 (1-2) ◽  
pp. 10-16 ◽  
Author(s):  
Meng Li ◽  
Fei Chen ◽  
Cui-Ping Liu ◽  
Dong-Mei Li ◽  
Xiang Li ◽  
...  

2011 ◽  
Vol 672 (1-3) ◽  
pp. 113-120 ◽  
Author(s):  
Qing-Ping Zuo ◽  
Shi-Kun Liu ◽  
Zuo-Jun Li ◽  
Bing Li ◽  
Yu-Lu Zhou ◽  
...  

2011 ◽  
Vol 252 (1) ◽  
pp. 18-27 ◽  
Author(s):  
Rong Zhang ◽  
Jianguo Sun ◽  
Liping Ma ◽  
Xiaolan Wu ◽  
Guoyu Pan ◽  
...  

Author(s):  
Nora A. Bawazeer ◽  
Hani Choudary ◽  
Mazin A. Zamzami ◽  
Wesam H. Abdulaal ◽  
Mustafa Zeyadi ◽  
...  

1997 ◽  
Vol 77 (05) ◽  
pp. 1014-1019 ◽  
Author(s):  
W Craig Hooper ◽  
Donald J Phillips ◽  
Bruce L Evatt

SummaryWe have recently demonstrated that the proinflammatory cytokine, interleukin-6 (IL-6), could upregulate the production of protein S in the human hepatoma cell line, HepG-2, but not in endothelial cells. In this study, we have demonstrated that the combination of exogenous IL-6 and soluble IL-6 receptor (sIL-6R) could significantly upregulate protein S production in both primary human umbilical vein endothelial cells (HUVEC) and in the immortalized human microvascular endothelial cell line, HMEC-1. The IL-6/sIL-6R complex was also able to rapidly induce tyrosine phosphorylation of the IL-6 transducer, gpl30. Neutralizing antibodies directed against either IL-6 or gpl30 blocked protein S upregulation by the IL-6/sIL-6R complex. It was also observed that exogenous sIL-6R could also upregulate protein S by forming a complex with IL-6 constitutively produced by the endothelial cell. Two other cytokines which also utilize the gpl30 receptor, oncostatin M (OSM) and leukemia inhibitory factor (LIF), were also able to upregulate endothelial cell protein S. This study demonstrates a mechanism that allows endothelial cells to respond to IL-6 and also illustrates the potential importance of circulating soluble receptors in the regulation of the anticoagulation pathway.


Sign in / Sign up

Export Citation Format

Share Document