Fig. 6. Co-expression of Adamts2 and Col3a1, and deficiency of
procollagen III processing in Adamts2-/- mice.
(A,B) Adamts2 is co-expressed with Col3a1 in
the arterial wall, as shown at two developmental stages: 12.5 dpc carotid
artery (A) and 17.5 dpc pulmonary artery (B). L, lung. (C) Expression
of Col3a1 and Adamts2 in lung. Note the expression in lung
mesnchyme but not in the epithelium of bronchial tubes (asterisk). (D)
Co-expression of Adamts2 and Col3a1 in the mesenchyme of the
palate (P). Adamts2 is also expressed in the perichondrium of the
basisphenoid (BS), at which location Col3a1 is absent. (E)
Co-expression of Adamts2 and Col3a1 in the peritoneum lining
the liver (L, arrow), and mesentery of the gut (G) and pancreas (Pa).
(F) Co-expression of Adamts2 and Col3a1 within the
subepithelial layer of the developing urinary bladder. Scale bar: 100 µm.
In D-F, Adamts2 expression is weaker than in lung and arteries, and
Col3a1 expression is also significantly weaker and more dispersed.
(G) Defective procollagen III processing in tissues from
Adamts2-/- mice. Western blot analysis of procollagen
isolated from mouse tissues with 0.15 M NaCl is shown. The tissue origin of
the sample and the respective genotype is shown above each lane; procollagen
III and collagen III molecular species are indicated on the left. Scanning
densitometry of the different collagen III signals was used to calculate the
proportion of fully processed molecules in the various tissues (lower panel).
(H) Defective procollagen III processing in newly synthesized collagen
in Adamts2-/- mice. Protein was extracted from sponge
granulomas and western blotting used to define the molecular species of
procollagen III that were present. Sponge granulomas from two
Adamts2-/- mice and their wild-type littermates are shown.
Scale bar: 100 µm.