Radial Construction of an Arterial Wall

SummarySome of the most serious diseases involve altered size and structure of the arterial wall. Elucidating how arterial walls are built could aid understanding of these diseases, but little is known about how concentric layers of muscle cells and the outer adventitial layer are assembled and patterned around endothelial tubes. Using histochemical, clonal, and genetic analysis in mice, here we show that the pulmonary artery wall is constructed radially, from the inside out, by two separate but coordinated processes. One is sequential induction of successive cell layers from surrounding mesenchyme. The other is controlled invasion of outer layers by inner layer cells through developmentally regulated cell reorientation and radial migration. We propose that a radial signal gradient controls these processes and provide evidence that PDGF-B and at least one other signal contribute. Modulation of such radial signaling pathways may underlie vessel-specific differences and pathological changes in arterial wall size and structure.Video Abstrac

Phase formation in the Pt/InP thin film system

InP substrates with 40nm metal films of Pt were encapsulated in SiO{sub 2}, and isochronally annealed up to 600{degrees}C in flowing forming gas. The composition and morphology of the phases that formed were studied using x-ray diffraction, Rutherford Backscattering, and transmission electron microscopy. Results show that the Pt/InP system begins interacting at 300{degrees}C. TEM analysis of the 350{degrees}C anneal shows unreacted Pt and additional polycrystalline phases, with no observed orientation relationship with the substrate. The Pt layer has been completely consumed by 400{degrees}C, with a uniform reacted layer indicated by RBS. At high temperatures (between 500{degrees}C and 600{degrees}C), the reaction products are PtIn{sub 2} and PtP{sub 2}. The two phases show a tendency for phase separation, with a higher concentration of PtP{sub 2} at the InP/reacted layer interface. The phosphide phase also shows a preferred orientation relationship with the substrate. 14 refs., 5 figs

The fibronectin leucine-rich repeat transmembrane protein Flrt2 is required in the epicardium to promote heart morphogenesis

The epicardium, the outermost tissue layer that envelops the developing heart and provides essential trophic signals for the myocardium, derives from the pro-epicardial organ (PEO). Two of the three members of the Flrt family of transmembrane glycoproteins, Flrt2 and Flrt3, are strongly co-expressed in the PEO. However, beginning at around day 10 of mouse development, following attachment and outgrowth, Flrt3 is selectively downregulated, and only Flrt2 is exclusively expressed in the fully delaminated epicardium. The present gene-targeting experiments demonstrate that mouse embryos lacking Flrt2 expression arrest at mid-gestation owing to cardiac insufficiency. The defects in integrity of the epicardial sheet and disturbed organization of the underlying basement membrane closely resemble those described in Flrt3-deficient embryos that fail to maintain cell-cell contacts in the anterior visceral endoderm (AVE) signalling centre that normally establishes the A-P axis. Using in vitro and in vivo reconstitution assays, we demonstrate that Flrt2 and Flrt3 are functionally interchangeable. When acting alone, either of these proteins is sufficient to rescue functional activities in the AVE and the developing epicardium