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Submitted on April 10, 2003
Accepted on May 23, 2003
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1 Laboratoire de Biologie Moléculaire et de Génie Génétique, Université de Liège, Allée du 6 Août B6A, B-4000 Liège, Belgium, * Génétique Humaine, Université de Liège, Avenue de l'Hôpital, 13 B35, B-4000 Liège, Belgium, Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California School of Medicine, San Francisco, California 94143, USA
* To whom correspondence should be addressed. E-mail: jmartial{at}ulg.ac.be.
We have previously shown that the 16-kDa N-terminal fragment of human PRL (16K hPRL) has antiangiogenic properties, including the ability to induce apoptosis in vascular endothelial cells. Here, we examined whether the NF-
B signaling pathway was involved in mediating the apoptotic action of 16K hPRL in bovine adrenal cortex capillary endothelial (BACE) cells. In a dose-dependent manner, treatment with 16K hPRL induced IB-
degradation permitting translocation of NF-B to the nucleus and reporter gene activation. Inhibition of NF-B activation by overexpression of a non-degradable IB- mutant or treatment with NF-B inhibitors blocked 16K hPRL-induced apoptosis. Treatment with 16K hPRL activated the initiator caspases 8 and 9 and the effector caspase 3, all of which were essential for stimulation of DNA fragmentation. This activation of the caspases cascade by 16K hPRL was also NF-B-dependent. These findings support the conclusion that NF-B signaling plays a central role in 16K hPRL-induced apoptosis in vascular endothelial cells.
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