THE DIADENOSINE POLYPHOSPHATES AP(3)A AND AP(4)A AND ADENOSINE-TRIPHOSPHATE INTERACT WITH GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR TO DELAY NEUTROPHIL APOPTOSIS - IMPLICATIONS FOR NEUTROPHIL PLATELET INTERACTIONS DURING INFLAMMATION

Citation
L. Gasmi et al., THE DIADENOSINE POLYPHOSPHATES AP(3)A AND AP(4)A AND ADENOSINE-TRIPHOSPHATE INTERACT WITH GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR TO DELAY NEUTROPHIL APOPTOSIS - IMPLICATIONS FOR NEUTROPHIL PLATELET INTERACTIONS DURING INFLAMMATION, Blood, 87(8), 1996, pp. 3442-3449
Citations number
44
Categorie Soggetti
Hematology
Journal title
BloodACNP
ISSN journal
00064971
Volume
87
Issue
8
Year of publication
1996
Pages
3442 - 3449
Database
ISI
SICI code
0006-4971(1996)87:8<3442:TDPAAA>2.0.ZU;2-O
Abstract
Incubation of neutrophils with cytokines such as granulocyte macrophag e colony-stimulating factor (GM-CSF) delays their loss of function and changes in cellular morphology that are characteristic of apoptosis. Adenosine triphosphate (ATP) and the diadenosine polyphosphates Ap(4)A and Ap(3)A were almost as effective as GM-CSF in delaying neutrophil apoptosis. The nucleotides could thus preserve cellular morphology, pr otect against chromatin fragmentation, and preserve functions such as NADPH oxidase activity and expression of CD16. Moreover, addition of A TP, Ap(3)A, and Ap(4)A together with GM-CSF resulted in more pronounce d protection from apoptosis than was observed during incubation with e ither the cytokine or the nucleotides alone. Because ATP, Ap(3)A, and Ap(4)A may be secreted from activated platelets, these observations su ggest that platelet-derived products, perhaps acting in combination wi th endothelial-derived or immune cell-derived cytokines, can regulate neutrophil function during certain types of inflammation. (C) 1996 by The American Society of Hematology.