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Blood, Vol. 96 No. 1 (July 1), 2000:
pp. 176-181
Bactericidal/permeability-increasing protein (BPI) inhibits
angiogenesis via induction of apoptosis in vascular endothelial cells
Daisy W. J. van der Schaft,
Elly A. H. Toebes,
Judith R. Haseman,
Kevin H. Mayo, and
Arjan W. Griffioen
From the Tumor Angiogenesis Laboratory, Department of
Internal Medicine, University Hospital Maastricht, Maastricht,
The Netherlands; and the Department of Biochemistry, Molecular Biology
and Biophysics, University of Minnesota Health Sciences Center,
Minneapolis, Minnesota.
Bactericidal/permeability-increasing protein (BPI) has been known
for some time to function in killing bacteria and in neutralizing the
effects of bacterial endotoxin lipopolysaccharide. In the present
study, BPI is found to be a novel endogenous inhibitor of angiogenesis.
Within the sub-µM range, BPI shows a
concentration-dependent inhibition of endothelial cell (EC)
proliferation that is mediated by cell detachment and subsequent
induction of apoptosis. As measured by flow cytometric analysis of the
percentage of subdiploid cells, apoptosis induction was half-maximal at
about 250 nmol/L BPI. Apoptosis was confirmed by quantification of
cells with nuclear fragmentation. Apoptosis was found to be EC
specific. In an in vitro collagen gel-based angiogenesis assay, BPI at
1.8 µmol/L inhibited tube formation by 81% after only 24 hours.
Evidence for in vivo inhibition of angiogenesis was obtained, using the chorioallantoic membrane assay in which BPI was seen to be
significantly effective at concentrations as low as 180 nmol/L. This
newly discovered function of BPI might provide a possible therapeutic
modality for the treatment of various pathologic disorders that depend on angiogenesis.
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