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Fig. 6. Cts8 causes vascular disintegration associated with
perivascular smooth muscle degradation. (A) Phenotype of E10.5
tgCts8 conceptuses upon ubiquitous activation of the
transgene (Sox2-Cre.tgCts8). No mature vitelline vessels
are observed. (B) Wild-type E10.5 embryo and ubiquitously activated
tgCts8 embryos (Sox2-Cre.tgCts8 and
CMV-Cre.tgCts8) at E10.5 (left-hand panels) and E9.5
(right-hand panels). Transgenic embryos are severely retarded and display an
inflated amnion (arrowheads), pericardial oedema (arrows) and lack of normal
heart chamber formation. Asterisks indicate the occurrence of blood pools.
(C) Yolk sac phenotype of Cts8-overexpressing
(Sox2-Cre.tgCts8) conceptuses. Pecam/CD31-positive
endothelial cells are present in transgenic samples; however, spaces between
the endodermal and mesodermal layers are dilated. Smooth muscle 
-actin
(SMA) staining surrounds vessels in wild-type yolk sacs, but is absent from
transgenic samples (arrowheads). (D,E) Laminin (Lam) and smooth
muscle -actin (SMA) staining on consecutive sections (D) and by double
immunofluorescence (E) of chorioallantoic vessels in the E9.5 placenta.
Laminin staining reveals disorganized vessel structures that lack smooth
muscle cells in transgenic samples (Sox2-Cre.tgCts8).
Arrows indicate vessel structures that display a striking reduction of SMA
staining in transgenic samples. The arrowhead indicates a site of vessel
rupture where blood cells (round, DAPI positive) can be seen exiting into the
surrounding tissue. (F) Quantitative RT-PCR analysis of SMA mRNA levels
in embryos (E) and placentas (P). (G) Consecutive sections of E9.5
placentas stained for Cts8 by RNA in situ hybridization (blue) and
SMA by immunohistochemistry (brown) showing lack of SMA in the vicinity of
Cts8-expressing giant cells. Scale bars: 1 mm in A; 500 µm in B;
50 µm in C; 50 µm in D; 100 µm in E; 500 µm in G.
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