Early postnatal lethality and cardiovascular defects in CXCR7-deficient mice
Version of Record online: 28 APR 2008
Copyright © 2008 Wiley-Liss, Inc.
Volume 46, Issue 5, pages 235–245, May 2008
How to Cite
Gerrits, H., van Ingen Schenau, D. S., Bakker, N. E.C., van Disseldorp, A. J.M., Strik, A., Hermens, L. S., Koenen, T. B., Krajnc-Franken, M. A.M. and Gossen, J. A. (2008), Early postnatal lethality and cardiovascular defects in CXCR7-deficient mice. Genesis, 46: 235–245. doi: 10.1002/dvg.20387
- Issue online: 28 APR 2008
- Version of Record online: 28 APR 2008
- Manuscript Accepted: 3 FEB 2008
- Manuscript Revised: 18 DEC 2007
- Manuscript Received: 25 JUN 2007
- N.V. Organon
CXCR7 is a G-protein coupled receptor that was recently deorphanized and shown to have SDF1 and I-TAC as high affinity ligands. Here we describe the characterization of CXCR7-deficient mice that were generated to further investigate the function of this receptor in vivo. Expression analysis using a LacZ reporter knockin revealed that postnatally Cxcr7 was specifically expressed in cardiomyocytes, vascular endothelial cells of the lung and heart, the cerebral cortex and in osteocytes of the bone. Adult tissues revealed high expression in cardiomyocytes and osteocytes. The observation that 70% of the Cxcr7−/− mice died in the first week after birth coincides with expression of Cxcr7 in vascular endothelial cells and in cardiomyocytes. An important role of CXCR7 in the cardiovascular system was further supported by the observation that hearts of the Cxcr7−/− mice were enlarged, showed myocardial degeneration and fibrosis of postnatal origin, and hyperplasia of embryonic origin. Despite high expression in osteocytes no apparent bone phenotype was observed, neither in combination with ovariectomy nor orchidectomy. Thus as CXCR7 does not seem to play an important role in bone our data indicate an important function of CXCR7 in the cardiovascular system during multiple steps of development. genesis 46:235–245, 2008. © 2008 Wiley-Liss, Inc.