C.E. Eyler and T. Jackson contributed equally to this work.
β2-Adrenergic receptor and adenylate cyclase gene polymorphisms affect sickle red cell adhesion
Article first published online: 6 MAR 2008
© 2008 The Authors
British Journal of Haematology
Volume 141, Issue 1, pages 105–108, April 2008
How to Cite
Eyler, C. E., Jackson, T., Elliott, L. E., De Castro, L. M., Jonassaint, J., Ashley-Koch, A. and Telen, M. J. (2008), β2-Adrenergic receptor and adenylate cyclase gene polymorphisms affect sickle red cell adhesion. British Journal of Haematology, 141: 105–108. doi: 10.1111/j.1365-2141.2008.07008.x
- Issue published online: 6 MAR 2008
- Article first published online: 6 MAR 2008
- Received 4 October 2007; accepted for publication 19 November 2007
- sickle cell disease;
- red blood cell (erythrocyte);
- cyclic adenosine monophosphate.
Sickle red cell (SS RBC) adhesion is thought to contribute to sickle cell disease (SCD) pathophysiology. SS RBC adhesion to laminin increases in response to adrenaline stimulation of β2-adrenergic receptors (β2ARs) and adenylate cyclase (ADCY6), and previous evidence suggests such activation occurs in vivo. We explored whether polymorphisms of the β2AR and ADCY6 genes (ADRB2 and ADCY6, respectively) affect RBC adhesion to laminin. We found that the β2AR arg16gly substitution and two non-coding ADCY6 polymorphisms were associated with elevated adhesion. We postulate that ADRB2 and ADCY6 polymorphisms may influence SCD severity through the mechanism of RBC adhesion.