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Prepublished online as a Blood First Edition Paper on August 15, 2002; DOI 10.1182/blood-2002-03-0768.
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Blood, 1 January 2003, Vol. 101, No. 1, pp. 186-193
IMMUNOBIOLOGY
Transendothelial migration leads to protection from
starvation-induced apoptosis in CD34+CD14+
circulating precursors: evidence for PECAM-1 involvement through
Akt/PKB activation
Elisabetta Ferrero,
Daniela Belloni,
Paola Contini,
Chiara Foglieni,
Maria Elena Ferrero,
Monica Fabbri,
Alessandro Poggi, and
Maria Raffaella Zocchi
From the Laboratory of Tumor Immunology, the Human
Virology Unit, Dibit, and the Unit of Human Immunology, Dibit, IRCCS
San Raffaele, the Department of General Pathology, University of Milan,
Italy; the Laboratory of Immunology, National Cancer Research
Institute, and the Laboratory of Clinical Immunology, Department of
Internal Medicine (DIMI), University of Genoa, Italy.
In the present paper we show that transendothelial migration of a
subset of CD14+ circulating leukocytes, coexpressing the
CD34 precursor marker, leads to protection from the apoptosis that
follows growth factor(s) withdrawal. The resistance of this cell subset
to starvation-induced programmed cell death, lasting from 48 to 96 hours, is accompanied by a rise of mitochondrial adenosine triphosphate
(ATP), a high nicotinamide adenine dinucleotide (NAD)/reduced
nicotinamide adenine dinucleotide (NADH) ratio, and by the
up-regulation of expression of the antiapoptotic proteins Bcl-2 and
Bcl-X, together with an increase in the cytoplasmic, inactive, form of
Bax. This suggests that protection from apoptosis is due to the
preservation of mitochondrial function(s). Interestingly, ligation of
the platelet endothelial cell adhesion molecule-1 (PECAM-1), which
drives CD14+CD34+ transendothelial migration,
leads to an increase in Bcl-2 A1 and Bcl-X intracellular content, and
to protection from starvation-induced apoptosis. This event is
dependent on the engagement of phosphatidylinositol-3 kinase
and activation of Akt/PKB that is known to contribute to Bcl-2 and
Bcl-X induction. These data point to a critical role of endothelium in
preventing the apoptotic program triggered by starvation, possibly
inducing a prolonged survival of antigen presenting cell precursors, in
order to allow recirculation of these cells and localization to the
site of priming of T lymphocytes.
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