Detrimental effects of adenosine signaling in sickle cell disease View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-01

AUTHORS

Yujin Zhang, Yingbo Dai, Jiaming Wen, Weiru Zhang, Almut Grenz, Hong Sun, Lijian Tao, Guangxiu Lu, Danny C Alexander, Michael V Milburn, Louvenia Carter-Dawson, Dorothy E Lewis, Wenzheng Zhang, Holger K Eltzschig, Rodney E Kellems, Michael R Blackburn, Harinder S Juneja, Yang Xia

ABSTRACT

Hypoxia can act as an initial trigger to induce erythrocyte sickling and eventual end organ damage in sickle cell disease (SCD). Many factors and metabolites are altered in response to hypoxia and may contribute to the pathogenesis of the disease. Using metabolomic profiling, we found that the steady-state concentration of adenosine in the blood was elevated in a transgenic mouse model of SCD. Adenosine concentrations were similarly elevated in the blood of humans with SCD. Increased adenosine levels promoted sickling, hemolysis and damage to multiple tissues in SCD transgenic mice and promoted sickling of human erythrocytes. Using biochemical, genetic and pharmacological approaches, we showed that adenosine A(2B) receptor (A(2B)R)-mediated induction of 2,3-diphosphoglycerate, an erythrocyte-specific metabolite that decreases the oxygen binding affinity of hemoglobin, underlies the induction of erythrocyte sickling by excess adenosine both in cultured human red blood cells and in SCD transgenic mice. Thus, excessive adenosine signaling through the A(2B)R has a pathological role in SCD. These findings may provide new therapeutic possibilities for this disease. More... »

PAGES

79

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm.2280

DOI

http://dx.doi.org/10.1038/nm.2280

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1026064448

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21170046


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