Skip to main content
. Author manuscript; available in PMC: 2009 Jun 9.
Published in final edited form as: Development. 2008 Oct 16;135(22):3801–3811. doi: 10.1242/dev.025825

Fig. 7. Enhanced BMPR1A signaling upregulates both sclerostin and osteoclastogenesis.

Fig. 7

(A) Constitutively active Bmpr1a (caBmpr1a) mouse fetuses at E18.5 induced daily by TM injection from E13.5. Hematoxylin and Eosin staining showed moderately reduced thickness in the caBmpr1a calvariae (Cre+, caBmpr1a+) where levels of phosphorylated Smad1/5/8 (brown) were enhanced compared with littermate controls (Cre−, caBmpr1a+). Scale bars: 50 μm. (B) Expressions of Sost and the bone resorption markers Rankl and Opg assessed by QRT-PCR using caBmpr1a and control calvariae at E18.5. Values are expressed relative to control. (C) Relative ratio of Rankl to Opg calculated based on the expression levels in Fig. 7B. (D) Expressions of Sost, bone resorption markers, Rankl and Opg by QRT-PCR using rescued (black bar: Cre+, caBmpr1a+, Bmpr1a fx/fx) and littermate cKO (gray bar: Cre+, caBmpr1a−, Bmpr1a fx/fx) calvariae at E18.5. Values of rescued mice are expressed relative to littermate cKO mice. (E) Relative ratio of Rankl to Opg calculated based on expression levels in Fig. 7D. (F) Hematoxylin and Eosin staining of rescued and cKO calvariae at E18.5. Scale bars: 100 μm. Values in B–E are mean±s.d. from three independent experiments. Student’s t-test; *P<0.05.