The role of red blood cell S-nitrosation in nitrite bioactivation and its modulation by leucine and glucose. Redox Biol 2016 Aug;8:415-21
Date
05/09/2016Pubmed ID
27156251Pubmed Central ID
PMC4864376DOI
10.1016/j.redox.2016.04.004Scopus ID
2-s2.0-84964902419 (requires institutional sign-in at Scopus site) 19 CitationsAbstract
Previous work has shown that red blood cells (RBCs) reduce nitrite to NO under conditions of low oxygen. Strong support for the ability of red blood cells to promote nitrite bioactivation comes from using platelet activation as a NO-sensitive process. Whereas addition of nitrite to platelet rich plasma in the absence of RBCs has no effect on inhibition of platelet activation, when RBCs are present platelet activation is inhibited by an NO-dependent mechanism that is potentiated under hypoxia. In this paper, we demonstrate that nitrite bioactivation by RBCs is blunted by physiologically-relevant concentrations of nutrients including glucose and the important signaling amino acid leucine. Our mechanistic investigations demonstrate that RBC mediated nitrite bioactivation is largely dependent on nitrosation of RBC surface proteins. These data suggest a new expanded paradigm where RBC mediated nitrite bioactivation not only directs blood flow to areas of low oxygen but also to areas of low nutrients. Our findings could have profound implications for normal physiology as well as pathophysiology in a variety of diseases including diabetes, sickle cell disease, and arteriosclerosis.
Author List
Wajih N, Liu X, Shetty P, Basu S, Wu H, Hogg N, Patel RP, Furdui CM, Kim-Shapiro DBAuthor
Neil Hogg PhD Associate Dean, Professor in the Biophysics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
ErythrocytesGlucose
Humans
Leucine
Nitric Oxide
Nitrites
Nitrosation
Oxygen
Vasodilation
