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SOST expression is restricted to the great arteries during embryonic and neonatal cardiovascular development
Author(s) -
van Bezooijen Rutger L.,
DeRuiter Marco C.,
Vilain Nathalie,
Monteiro Rui M.,
Visser Annemieke,
van der WeePals Lianne,
van Munsteren Conny J.,
Hogendoorn Pancras C.W.,
Aguet Michel,
Mummery Christine L.,
Papapoulos Socrates E.,
Ten Dijke Peter,
Löwik Clemens W.G.M.
Publication year - 2007
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.21054
Subject(s) - biology , aorta , ascending aorta , wnt signaling pathway , anatomy , bone morphogenetic protein , great arteries , medicine , embryonic stem cell , endocrinology , microbiology and biotechnology , signal transduction , heart disease , gene , biochemistry
Spatial–temporal regulation of bone morphogenetic protein (BMP) and Wnt activity is essential for normal cardiovascular development, and altered activity of these growth factors causes maldevelopment of the cardiac outflow tract and great arteries. In the present study, we show that SOST , a Dan family member reported to antagonize BMP and Wnt activity, is expressed within the medial vessel wall of the great arteries containing smooth muscle cells. The ascending aorta, aortic arch, brachiocephalic artery, common carotids, and pulmonary trunk were all associated with SOST expressing smooth muscle cells, while the heart itself, including the valves, and more distal arteries, that is, pulmonary arteries, subclavian arteries, and descending aorta, were negative. SOST was expressed from embryonic day 15.5 up to the neonatal period. SOST expression, however, did not correspond with inhibition of Smad‐dependent BMP activity or β‐catenin–dependent Wnt activity in the great arteries. Activity of both signaling pathways was already down‐regulated before induction of SOST expression. Developmental Dynamics 236:606–612, 2007. © 2006 Wiley‐Liss, Inc.