Hyperactivation of p21^ras and PI3K cooperate to alter murine and human neurofibromatosis type 1–haploinsufficient osteoclast functions
J. Clin. Invest. Feng-Chun Yang, et al. 116:2880 doi:10.1172/JCI29092 [Go to this article.]

Figure 4
Effect of heterozygosity of Nf1 on osteoclast haptotaxis and F-actin content in response to recombinant murine M-CSF. (A) Haptotaxis of WT and Nf1^+/– osteoclasts in response to M-CSF. A representative photomicrograph (magnification, ×20) from 1 of 5 experiments. (B) Quantitative evaluation of migration in response to M-CSF. Results represent the mean ± SEM of 5 experiments. *P < 0.01, Nf1^+/– versus WT by Student’s t test. (C) Photomicrographs (magnification, ×10) of M-CSF–stimulated osteoclast adhesion to αVβ3. Genotypes and length of adhesion are indicated. (D) Quantitative evaluation (mean ± SEM; n = 5) of osteoclast adhesion 10–60 minutes following incubation with M-CSF. Genotypes and length of adhesion are indicated. *P < 0.01, Nf1^+/– versus WT osteoclasts by Student’s t test. (E) M-CSF–mediated F-actin polymerization. Osteoclasts were stimulated with 10 ng/ml M-CSF and fixed at the time points indicated. WT and Nf1^+/– cells were examined in triplicate. Results are expressed as mean channel fluorescence (MCF). **P < 0.001, Nf1^+/– osteoclasts versus WT osteoclasts by Student’s t test.