Patterns & Phenotypes
PDGF-B signaling is important for murine cardiac development: Its role in developing atrioventricular valves, coronaries, and cardiac innervation
Article first published online: 21 JAN 2008
Copyright © 2008 Wiley-Liss, Inc.
Volume 237, Issue 2, pages 494–503, February 2008
How to Cite
Van den Akker, N. M.S., Winkel, L. C.J., Nisancioglu, M. H., Maas, S., Wisse, L. J., Armulik, A., Poelmann, R. E., Lie-Venema, H., Betsholtz, C. and Gittenberger-de Groot, A. C. (2008), PDGF-B signaling is important for murine cardiac development: Its role in developing atrioventricular valves, coronaries, and cardiac innervation. Dev. Dyn., 237: 494–503. doi: 10.1002/dvdy.21436
- Issue published online: 21 JAN 2008
- Article first published online: 21 JAN 2008
- Manuscript Accepted: 5 DEC 2007
- Netherlands Heart Foundation. Grant Number: 2001B057
- heart development;
- coronary arteriogenesis;
- cardiac innervation
We hypothesized that PDGF-B/PDGFR-β-signaling is important in the cardiac contribution of epicardium-derived cells and cardiac neural crest, cell lineages crucial for heart development. We analyzed hearts of different embryonic stages of both Pdgf-b−/− and Pdgfr-β−/− mouse embryos for structural aberrations with an established causal relation to defective contribution of these cell lineages. Immunohistochemical staining for αSMA, periostin, ephrinB2, EphB4, VEGFR-2, Dll1, and NCAM was performed on wild-type and knockout embryos. We observed that knockout embryos showed perimembranous and muscular ventricular septal defects, maldevelopment of the atrioventricular cushions and valves, impaired coronary arteriogenesis, and hypoplasia of the myocardium and cardiac nerves. The abnormalities correspond with models in which epicardial development is impaired and with neuronal neural crest–related innervation deficits. This implies a role for PDGF-B/PDGFR-β-signaling specifically in the contribution of these cell lineages to cardiac development. Developmental Dynamics 237:494–503, 2008. © 2008 Wiley-Liss, Inc.