Article (Scientific journals)
The antiangiogenic factor 16K PRL induces programmed cell death in endothelial cells by caspase activation
Martini, J. F.; Piot, C.; Humeau, L. M. et al.
2000In Molecular Endocrinology, 14 (10), p. 1536-49
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Keywords :
Antibodies, Monoclonal/pharmacology; Apoptosis/*drug effects; Caspases/*metabolism; Cell Division/drug effects; Cell Line; DNA/metabolism; DNA Fragmentation/drug effects; Drug Contamination; Endothelium, Vascular/*cytology; Endotoxins/pharmacology; Enzyme Activation/drug effects; Escherichia coli; Female; Heat; Humans; Molecular Weight; Neovascularization, Physiologic/*drug effects; Peptide Fragments/immunology/*pharmacology; Prolactin/immunology/*pharmacology; Protein Denaturation; Proto-Oncogene Proteins c-bcl-2/metabolism; Receptors, Prolactin/physiology; Receptors, Somatotropin/physiology; Recombinant Proteins/pharmacology; Research Support, Non-U.S. Gov't; Trypsin/pharmacology
Abstract :
[en] We asked whether the antiangiogenic action of 16K human PRL (hPRL), in addition to blocking mitogen-induced vascular endothelial cell proliferation, involved activation of programmed cell death. Treatment with recombinant 16K hPRL increased DNA fragmentation in cultured bovine brain capillary endothelial (BBE) and human umbilical vein endothelial (HUVE) cells in a time- and dose-dependent fashion, independent of the serum concentration. The activation of apoptosis by 16K hPRL was specific for endothelial cells, and the activity of the peptide could be inhibited by heat denaturation, trypsin digestion, and immunoneutralization, but not by treatment with the endotoxin blocker, polymyxin-B. 16K hPRL-induced apoptosis was correlated with the rapid activation of caspases 1 and 3 and was blocked by pharmacological inhibition of caspase activity. Caspase activation was followed by inactivation of two caspase substrates, poly(ADP-ribose) polymerase (PARP) and the inhibitor of caspase-activated deoxyribonuclease (DNase) (ICAD). Furthermore, 16K hPRL increased the conversion of Bcl-X to its proapoptotic form, suggesting that the Bcl-2 protein family may also be involved in 16K hPRL-induced apoptosis. These findings support the hypothesis that the antiangiogenic action of 16K hPRL includes the activation of programmed cell death of vascular endothelial cells.
Disciplines :
Biochemistry, biophysics & molecular biology
Author, co-author :
Martini, J. F.
Piot, C.
Humeau, L. M.
Struman, Ingrid  ;  Université de Liège - ULiège > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire
Martial, Joseph ;  Université de Liège - ULiège > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire
Weiner, R. I.
Language :
English
Title :
The antiangiogenic factor 16K PRL induces programmed cell death in endothelial cells by caspase activation
Publication date :
2000
Journal title :
Molecular Endocrinology
ISSN :
0888-8809
eISSN :
1944-9917
Publisher :
The Endocrine Society, United States - Maryland
Volume :
14
Issue :
10
Pages :
1536-49
Peer reviewed :
Peer Reviewed verified by ORBi
Available on ORBi :
since 06 May 2009

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