Anat Embryol (2004) 208:219–224 DOI 10.1007/s00429-004-0396-z ORIGINAL ARTICLE S. Nimmagadda · P. G. Loganathan · J. Wilting · B. Christ · R. Huang Expression pattern of VEGFR-2 (Quek1) during quail development Accepted: 18 March 2004 / Published online: 20 May 2004  Springer-Verlag 2004 Abstract The growth and maintenance of the blood and lymphatic vascular systems is to a large extent con- trolled by members of the vascular endothelial growth factor (VEGF) family via the tyrosine kinase receptors (VEGFRs) expressed in angioblastic cells. Here, we analyzed the Quek1 (VEGFR-2) expression pattern by whole mount in situ hybridization during quail develop- ment. During early embryogenesis, Quek1 expression was detected at the caudal end of the blastoderm and primitive streak and in the head paraxial mesoderm. In somites, expression was observed from HH-stage 9 onwards in the dorsolateral region of both the forming and recently formed somites. During somite maturation, expression persists in the lateral portion of the somitic compartments, the dermomyotome and the sclerotome. Additionally, a second expression domain in the maturing somite was observed in the medial part of the sclerotome adjacent to the neural tube. This expression domain extended medi- ally and dorsally and surrounded the neural tube during later stages. In the notochord, expression was observed from HH-stage 23 onwards. In the limb bud, expression was initiated in the mesenchyme at HH-stage 17. During organogenesis, expression was detected in the pharyngeal arches and in the anlagen of the esophagus, trachea, stomach, lungs, liver, heart and gut. Expression was also seen in feather buds from day 7 onwards. Our results confirm the angiogenic potential of the mesoderm and suggest that VEGFR-2 expressing cells represent multiple pools of mesodermal precursors of the hematopoietic and angiopoietic lineages. Keywords Quek1 · VEGF · VEGFR-2 · Endothelial cells · Quail embryo Introduction During embryogenesis, mesodermal cells differentiate into endothelial precursor cells, which are called an- gioblasts. In situ differentiation of these angioblasts into endothelial cells that subsequently form immature blood vessels of a primary vascular plexus is referred to as vasculogenesis. Angiogenesis describes the subsequent growth, remodeling and maturation process, which leads to the formation of differentiated blood vessels and mostly takes its origin from existing vessels. The growth and maintenance of the blood and lymphatic vascular systems is to a large extent mediated by members of the vascular endothelial growth factor (VEGF) family via their tyrosine kinase receptors (VEGFRs) that are ex- pressed in angioblastic and endothelial cells (Ferrara, 2000). VEGF is known as a vascular permeability factor, as it promotes the extravasation of fluid and plasma proteins, including fibrin, from blood vessels (Dvorak et al. 1995). VEGF supports proliferation and survival of endothelial cells and induces the expression of anti- apoptotic proteins in endothelial cells (Alon et al. 1995; Benjamin et al. 1999). The VEGF family includes five members: VEGF, VEGF-B, VEGF-C, VEGF-D and PlGF (placenta growth factor). Endothelial tyrosine kinase receptors are of funda- mental importance for the transmission of both differen- tiation and angiogenic signals from the environment to the endothelium (Wilting et al. 2003). VEGFs bind with high affinity to five receptors: three receptor tyrosine kinases called VEGFR-1 (Flt-1), VEGFR-2 (Flk-1/KDR) and VEGFR-3 (Flt-4), as well as two non-kinase re- ceptors, neuropilin-1 (NRP-1) and NRP-2. All VEGFRs are characterized by seven extracellular immunoglobulin homology domains (Barleon et al. 1997; Davis-Smyth et al. 1996; Fuh et al. 1998; Makinen et al. 2001). VEGFR-2 influences angioblast differentiation (Shalaby et al. 1995). S. Nimmagadda · P. G. Loganathan · B. Christ ( ) ) · R. Huang Institute of Anatomy and Cell Biology II, University of Freiburg, Albertstrasse 17, 79104 Freiburg, Germany e-mail: bodo.christ@anat.uni-freiburg.de Tel.: +49-761-2035089 Fax: +49-761-2035091 J. Wilting Kinderklinik und Poliklinik, Universitätsklinik Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany