Neutrophils as Sources of Extracellular Nucleotides: Functional Consequences at the Vascular Interface

Eltzschig, Holger K.; MacManus, Christopher F.; Colgan, Sean P.

doi:10.1016/j.tcm.2008.01.006

« PreviousTrends in Cardiovascular Medicine
Volume 18, Issue 3 , Pages 103-107, April 2008

Neutrophils as Sources of Extracellular Nucleotides: Functional Consequences at the Vascular Interface

Holger K. Eltzschig
- Department of Anesthesiology and Intensive Care Medicine, University of Colorado Health Sciences Center, Denver, CO 80220, USA
- Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80220, USA
- Mucosal Inflammation Program, University of Colorado Health Sciences Center, Denver, CO 80220, USA
- Department of Anesthesio-logy, Tuebingen University Hospital, Tuebingen, Germany
Christopher F. MacManus
- Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80220, USA
- Mucosal Inflammation Program, University of Colorado Health Sciences Center, Denver, CO 80220, USA
Sean P. Colgan
- Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80220, USA
- Mucosal Inflammation Program, University of Colorado Health Sciences Center, Denver, CO 80220, USA
- Address correspondence to: Sean P. Colgan, PhD, Mucosal Inflammation Program, BRB Room 702, 4200 E 9th Ave Denver, CO 80220, USA. Tel.: (+1) 303 315 1064 (Office), (+1) 303 315 1068 (Lab)

Abstract

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.