The Baldwin laboratory has concentrated on delineating the molecular basis of vascular development in the mammalian embryo as an approach to understanding the etiology of congenital heart diseases. Laboratory efforts are based on the hypothesis that the developing vasculature provides important patterning information that directs subsequent cardiac and pulmonary morphogenetic events. Specific projects includes a focus on: 1) the role of endothelial cell adhesion molecules, particularly PECAM-1 in regulating vascular ontogeny, 2) the role of NFATc-1 in specification of endocardial development during early organogenesis, 3) the importance of BMP signaling in valvuloseptal morphogenesis and 4) the importance of endothelial RTK signaling in vascular morphogenesis both in utero and in the adult animal. A variety of techniques including in vitro cell culture, in situ whole mouse embryo culture, adenoviral mediated tissue specific gene delivery in situ and in utero, microarray screening, transgenic and traditional null mutation via homologous recombination, chimeric analysis by ES cell blastocyst complementation, and Cre-Lox mediated tissue specific and inducible gene deletion are being utilized to pursue these studies.

For more information about Dr. Baldwin visit his Vanderbilt Faculty Page

NEWEST PUBLICATIONS

NFATc1 identifies a population of proximal tubule cell progenitors.  2008 Journal of the American Society of Nephrology 20: 311-321

ndrg4 is required for normal myocyte proliferation during early cardiac development in zebrafish.  2008 Developmental Biology 317: 486-496

Fate mapping using Cited1-CreERT2 mice demonstrates that the cap mesenchyme contains self-renewing progenitor cells and gives rise exclusively to nephronic epithelia.  2008 Developmental Biology 313: 234-245