Neutrophils as sources of extracellular nucleotides: functional consequences at the vascular interface.
Nucleotide signaling is currently an area of intense investigation. Extracellular adenosine triphosphate (ATP) liberated during hypoxia or inflammation can either signal directly to purinergic receptors or, after phosphohydrolytic metabolism, can activate surface adenosine receptors. Given the association of polymorphonuclear leukocytes (PMNs) with adenine nucleotide/nucleoside signaling in the inflammatory milieu, it was recently demonstrated that PMNs actively release ATP via a connexin 43 hemichannel-dependent mechanism. Here, we review the mechanisms of ATP release and subsequent functional implications of ATP metabolism at the interface between PMN and vascular endothelial cells during inflammation and in hypoxia.
Eltzschig
Holger K
HK
Department of Anesthesiology and Intensive Care Medicine, University of Colorado Health Sciences Center, Denver, CO 80220, USA.
Macmanus
Christopher F
CF
Colgan
Sean P
SP
D000255:Adenosine Triphosphate / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D015687:Cell Hypoxia / Q000502:physiology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D018375:Neutrophil Activation / Q000502:physiology*; D009504:Neutrophils / Q000378:metabolism / Q000502:physiology*; D009711:Nucleotides / Q000378:metabolism*; D015398:Signal Transduction
D009711:Nucleotides; D000255:Adenosine Triphosphate