Nitric oxide: a key regulator of myeloid inflammatory cell apoptosis.
Apoptosis of inflammatory cells is a critical event in the resolution of inflammation, as failure to undergo this form of cell death leads to increased tissue damage and exacerbation of the inflammatory response. Many factors are able to influence the rate of apoptosis in neutrophils, eosinophils, monocytes and macrophages. Among these is the signalling molecule nitric oxide (NO), which possesses both anti- and proapoptotic properties, depending on the concentration and flux of NO, and also the source from which NO is derived. This review summarises the differential effects of NO on inflammatory cell apoptosis and outlines potential mechanisms that have been proposed to explain such actions.
Centre for Inflammation Research, Rayne Laboratory, University of Edinburgh, Medical School, Teviot Place, Edinburgh EH8 9AG, UK. e.l.taylor-2@sms.ed.ac.uk
E L
EL
Taylor
I L
IL
Megson
C
C
Haslett
A G
AG
Rossi
D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism*; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000378:metabolism; D022423:Myeloid Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000494:pharmacology / Q000627:therapeutic use
D018836:Inflammation Mediators; D020030:Nitric Oxide Donors; D009569:Nitric Oxide