Essential role of RSK2 in c-Fos–dependent osteosarcoma development
J. Clin. Invest. Jean-Pierre David, et al. 115:664 doi:10.1172/JCI22877 [
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Figure 3Molecular and cellular analysis of the bone defects in
Rsk2-deficient mice. (
A) Analysis of type I collagen (col I), osteocalcin (oc), osteopontin (op), and Phex expression in the cortical bone of 8-week-old wild-type and
Rsk2–/y littermates. (
B) Analysis of osteoid volume in 28-week-old wild-type and
Rsk2–/y littermates compared with
Hyp–/y mice (24 weeks old). *
P < 0.05. (
C) Analysis of RSK2 and ERK activation in primary osteoblast cultures stimulated by IGF-1. RSK2 and ERK activation was analyzed by blotting with phospho-specific antibodies, and the loading was controlled by reblotting with total ERK antibody. (
D) Proliferation curve of primary
Rsk2-deficient osteoblasts compared with wild-type. (
E) Determination of proliferation and apoptotic indices in
Rsk2-deficient and wild-type osteoblasts in vitro. Arrowheads indicate TUNEL-positive cells. Quantifications are indicated in the lower left corners. Magnification, ×10. (
F) In vitro differentiation of
Rsk2-deficient osteoblasts compared with wild-type. Alkaline phosphatase activity (ALP) and bone nodule mineralization by alizarin red staining (ALZ) are shown. Arrowheads indicate alizarin red–positive bone nodules. Magnification, ×5. (
G) Effect of IGF-1 on bone nodule mineralization by
Rsk2-deficient osteoblasts compared with wild-type.
