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 3
Increase in the number of myeloid progenitors and TRAP⁺ cells in response to varying concentrations of M-CSF and RANKL. (A) Increase in the number of CFU-Ms per femur in response to M-CSF. Data represent the mean ± SEM of 5 experiments. *P < 0.01, Nf1^+/– versus WT CFU-Ms by Student’s t test. (B and C) Evaluation of the ability of Nf1^+/– and WT BMMNCs to form osteoclasts in response to M-CSF (B) and RANKL (C). Data represent the mean ± SEM of TRAP⁺ cells/5 × 10⁴ LDMNCs from 5 experiments. ^#P < 0.01, Nf1^+/– versus WT TRAP⁺ cells. (D) Osteoclast DNA content of cultured WT osteoclast (left panel) and Nf1^+/– osteoclasts (right panel) was determined using fluorescence cytometry following PI staining. (E) Representative photomicrographs (magnification, ×20) of Nf1^+/– and WT osteoclasts in liquid culture. Arrows indicate selected osteoclasts. (F) Osteoclast survival was determined by calculating annexin V– and PI-negative cell populations. ^##P < 0.05 and **P < 0.01, Nf1^+/– versus WT osteoclasts.