Journal
TRENDS IN CARDIOVASCULAR MEDICINE
Volume 18, Issue 3, Pages 103-107Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcm.2008.01.006
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL060569] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [P01DE013499, P50DE016191] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK050189, R37DK050189, R29DK050189] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL060569, R01 HL060569-10A2, R01 HL060569-09, HL 60569] Funding Source: Medline
- NIDCR NIH HHS [P01 DE013499-010003, DE 016191, P01 DE013499-020003, P01 DE013499-02S10003, P01 DE013499-050003, P01 DE013499-030003, P01 DE013499-040003, P50 DE016191, P01 DE013499] Funding Source: Medline
- NIDDK NIH HHS [R01 DK050189, R37 DK050189, R29 DK050189-05, DK 50189, R29 DK050189] Funding Source: Medline
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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.
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