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. Author manuscript; available in PMC: 2014 Oct 26.
Published in final edited form as: Arthritis Rheum. 2012 Oct;64(10):3334–3343. doi: 10.1002/art.34556

Figure 6. CD248 signals via the platelet-derived growth factor receptor (PDGFR) to maintain osteoblasts in an immature state.

Figure 6

A, Confocal microscopy images of newborn mouse tibiae show the colocalization of CD248 and PDGFRα (left), and the colocalization of CD248, PDGFRα, and alkaline phosphatase (Alk Phos) (merged image; right). B, Total ERK (t-ERK) and phosphorylated ERK (p-ERK) were assessed by Western blotting in osteoblasts from WT and CD248−/− mouse tibiae exposed to PDGF-BB for 0, 1, or 5 minutes. C, Real-time polymerase chain reaction was performed to analyze c-fos expression, normalized to the values for GAPDH, in osteoblasts from WT and CD248−/− mice after stimulation with PDGF-BB. Results are the mean ± SD fold change in 3 samples per group, relative to that in control, untreated cultures (set at 1). D, Proliferation of WT and CD248−/− mouse osteoblasts was assessed by MTT proliferation assay after 6 days of stimulation with PDGF-BB or transforming growth factor β (TGFβ). Results, at an absorbance at 550 nm, are the mean ± SEM of 3 samples per group, normalized to the control, untreated cell response. E, Results of in vitro mineralization assays, with or without PDGF-BB, show that bone nodule formation was inhibited at all time points after stimulation with PDGF-BB in WT mouse osteoblasts, but not in CD248−/− mouse osteoblasts. Bars show the mean ± SEM of 6 samples per group. Experiments were repeated twice; representative results are shown. * = P < 0.05; *** = P < 0.001, by Student’s t-test. NS = not significant.