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. Author manuscript; available in PMC: 2010 Jan 1.
Published in final edited form as: Dev Biol. 2008 Oct 17;325(1):82–93. doi: 10.1016/j.ydbio.2008.09.031

Figure 1. PlexinD1 is broadly expressed in late embryonic development and is required for Sema3A-mediated endothelial cell migration in vitro.

Figure 1

PlexinD1 mRNA was detected by in situ hybridization (red signal) in the heart and vascular endothelium (A, arrow), forebrain (C), dorsal root ganglia and adrenal gland (D, arrow), lung mesenchyme (G), and the ossification centers of vertebral bodies (J, arrow). Adjacent sections were stained for vWF (B, H), neurofilament (2H3) (E) and tyrosine hydroxylase (F) by immunohistochemistry and wnt2 by in situ hybridization (I). fb, fore brain; gV, trigeminal ganglion; cp, choroid plexus; ad, adrenal gland; drg, dorsal root ganglion; oc, ossification center. Scale bars equal to 500 μm in panel C and 100 μm in other panels. (K) Boyden chamber assays reveal the motility of primary endothelial cells (PEC) from plexinD1−/− mouse is impaired as determined by calcein AM emission (see methods). PECs from plexinD1+/− (het, dotted line) and plexinD1−/− (ko, solid line) pups were assessed at basal condition (Ctrl), and when soluble Sema3A was added to the upper chamber (3A). (L) Aortic ring assays reveal reduced responsiveness of plexinD1−/− aortic explants to Sema3A. The explants were incubated in complete medium (green) or complete medium plus Sema3A (red). Results are expressed as absolute outgrowth in mm: 1.26±0.19 mm (in control medium), and 1.02±0.18 mm (in SEMA3A conditional medium) from wild type and plexinD1+/− explants (n=10). From plexinD1−/− explants (n=7), the absolute outgrowth is 1.17±0.13 mm (in control medium) and 1.23±0.17 mm (in SEMA3A conditional medium). Representative images of aortic ring explants are shown in Supplemental Figure 1. n.s., not significant.