Association between P2X7 Receptor Polymorphisms and Bone Status in Mice.pdfVIP

Hindawi Publishing Corporation Journal of Osteoporosis Volume 2012, Article ID 637986, 10 pages doi:10.1155/2012/637986 Research Article Association between P2X7 Receptor Polymorphisms and Bone Status in Mice Susanne Syberg,1, 2 Peter Schwarz,1, 2 Solveig Petersen,1, 2 Thomas H. Steinberg,3 Jens-Erik Beck Jensen,2 Jenni Teilmann,2 and Niklas Rye Jørgensen1, 2 1 Research Centre of Ageing and Osteoporosis, Departments of Diagnostics and Medicine, Glostrup University Hospital, 2600 Glostrup, Denmark 2 Osteoporosis and Bone Metabolic Unit, Departments of Endocrinology and Clinical Biochemistry, Hvidovre University Hospital, 2650 Hvidovre, Denmark 3 Department of Internal Medicine, Washington University School of Medicine and the St. Louis Veterans Aff airs Medical Center, St. Louis, MO 63110, USA Correspondence should be addressed to Susanne Syberg, syberg@ruc.dk Received 31 March 2012; Accepted 28 May 2012 Academic Editor: Elena Adinolfi Copyright © 2012 Susanne Syberg et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Macrophages from mouse strains with the naturally occurring mutation P451L in the purinergic receptor P2X7 have impaired responses to agonists (1). Because P2X7 receptors are expressed in bone cells and are implicated in bone physiology, we asked whether strains with the P451L mutation have a different bone phenotype. By sequencing the most common strains of inbred mice, we found that only a few strains (BALB, NOD, NZW, and 129) were harboring the wild allelic version of the mutation (P451) in the gene for the purinergic receptor P2X7. The str