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Prepublished online as a Blood First Edition Paper on August 15, 2002; DOI 10.1182/blood-2002-03-0768.
Submitted March 13, 2002
Accepted July 30, 2002
Transendothelial migration leads to protection from starvation-induced apoptosis in CD34+ CD14+ circulating prescursors: 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*
Lab. Tumor Immunology Int Med, Sci Inst San Raffaele, Milan, Italy
Lab. Clinical Immunology DIMI, University of Genoa, Genoa, Italy
Human Virology Unit, Sci Inst San Raffaele, Milan, Italy
General Pathology, University of Milan, Milan, Italy
Human Immunology Unit DiBit, Sci Inst San Raffaele, Milan, Italy
Lab. Immunology, National Cancer Research Institute, Genoa, Italy
* Corresponding author; email: zocchi.maria{at}hsr.it.
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 which 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 ATP, a high NAD/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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