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Fig. 6. Suppressed expression of sclerostin by loss of BMP signaling ex
vivo. (A) Newborn mouse calvariae were cultured for 5 days treated
with 4OH-TM (100 ng/ml). (a) Confirmation of Cre activity in the
calvariae from CreER:R26R mice assessed by β-gal
staining. (b) Upregulation of canonical Wnt signaling in the calvariae
from CreER:Bmpr1afx/fx:TOPGAL mice assessed by
β-gal staining. Broken lines, areas of parietal bones (P). (c)
Expression of Wnt inhibitors Sost, Dkk1, Dkk2 and Lrp5
assessed by QRT-PCR. (d) Expressions of bone resorption markers
Mmp9, Ctsk, TRAP and Bmpr1a. Values are expressed relative
to those of wild type (Cre-, TM-). (B) Sclerostin treatment of
wild-type (WT+Scl) and cKO (cKO+Scl) calvariae ex vivo. The ratio of
β-gal to DAPI-positive cells was evaluated from 50 fields in frontal
sections (n=3, in each condition). Broken line, parietal bones. Scale
bars: 50 µm. (C) Expression of bone resorption markers
Rankl and Opg, and relative ratio of Rankl to
Opg using wild-type and cKO calvariae in sclerostin treated versus
untreated groups. Values are expressed relative to those of wild type without
sclerostin treatment. (D) TRAP staining of cKO calvariae treated with
sclerostin and non-treated ex vivo. Values in A-C represent mean±s.d.
from three independent experiments. Student's t-test;
*P<0.05.
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