Erratum to: Wnt Signaling Inhibits Osteoclast Differentiation by Activating Canonical and Noncanonical cAMP/PKA Pathways: Wnt INHIBITS OC DIFFERENTIATION BY CANONICAL/NONCANONICAL PATHWAYS (Journal of Bone and Mineral Research, (2016), 31, 1, (65-75), 10.1002/jbmr.2599)

A reader of the JBMR informed the editors about concern regarding two figures in the article by Weivoda et al The authors wish to acknowledge that an error was made in the article; the figure legend for Fig. was incomplete, and Fig. was inadvertently reported incorrectly. The figure legends below show the corrections in bold text. 1 (Figure presented.) Wnt receptors are expressed in the osteoclast lineage and Wnt signaling in early osteoclasts suppresses osteoclast differentiation. (A) Bone marrow–derived osteoclast precursors were harvested (D0) or cultured with RANKL and M-CSF to obtain osteoclasts on day 4 (D4) and protein lysates were examined for Wnt receptor expression. (B, C) Cells were fixed on day 4, TRAP stained, and quantitated as detailed in the Methods section. (B) Osteoclast precursors were treated with vehicle (VEH) or the indicated Wnt3a concentration throughout differentiation culture. (C) Osteoclast precursors were cultured with either vehicle or 100 ng/mL Wnt3a beginning on the indicated day of culture. (D) Osteoclast precursors were cultured with either vehicle or 100 ng/mL Wnt5a beginning on the indicated day of culture. (E) Osteoclast precursors were serum starved for 60 minutes, and treated with vehicle (Veh) or 100 ng/mL Wnt3a for 15 minutes. 40 mg of cell lysate was analyzed by Western blot analysis for phosphorylated NFATc1 and tubulin. (F) Osteoclast precursors were cultured for 6 hours with RANKL and M-CSF with either vehicle (Veh) or 100 ng/mL Wnt3a before nuclear isolation and extraction. 5 mg of nuclear extract was probed by Western blot analysis for total NFATc1 and lamin. (G) Osteoclast precursors were cultured as in E. 40 mg of cell lysate was analyzed by Western blot analysis for total NFATc1 and tubulin. (H) Osteoclast precursors differentiated for the indicated time were serum starved for 60 minutes, and treated with vehicle (Veh) or 100 ng/mL Wnt3a for 15 minutes. 40 mg of cell lysate was analyzed by Western blot analysis for phosphorylated NFATc1 and tubulin. *P < 0.05 compared to vehicle treatment (B) or *P < 0.01 compared to vehicle treatment (C) 2 (Figure presented.) Wnt3a activates canonical Wnt signaling in osteoclast precursors to suppress osteoclast differentiation. (A) Osteoclast precursors were serum starved for 60 minutes, and treated with vehicle (Veh) or 100 ng/mL Wnt3a for 15 minutes (samples from the experiment described in Fig. E). 40 mg of cell lysate was analyzed by Western blot analysis for active β-catenin and tubulin. (B) Osteoclast precursors were cultured with vehicle or 100 ng/mL Wnt3a treatment for 6 hours before nuclear isolation and extractions. 5 mg of nuclear extract was probed by Western blot analysis for total β-catenin and actin. (C) Osteoclast precursors were cultured with either sodium chloride (NaCl) (salt control), lithium chloride (LiCl), vehicle DMSO (Veh, GSK Inhib control), or a GSK3-β inhibitor (GSK Inhib) throughout culture. Cells were fixed on day 4, TRAP stained, and quantitated as detailed in the Methods section. Results are the ratio of Wnt3a treated to vehicle treated osteoclast numbers. *P < 0.05 compared to vehicle or control treatment. (D, E) Osteoclast precursors from control littermate or LrpRankCre mice (D) or βcat flox osteoclast precursors treated with control or Cre-adenovirus (MOI = 100) (E) were cultured 15 minutes with RANKL and M-CSF and either vehicle (Veh) or 100 ng/mL Wnt3a. 40 mg of cell lysate was analyzed by Western blot analysis for phosphorylated and total NFATc1 In the legend for Fig, the description of the experimental sample for Fig. E was incorrect in that the serum starvation part of the protocol was omitted. Because of this error, it can be concluded that they are separate experiments from Fig. A. This figure legend has been corrected below. The incorrect bands were used in Fig. E due to an inadvertent error. The original data were provided to the Editors for review, and the corrected Fig. E is shown below as well as the corrected caption for Fig. These corrections do not change the outcome of the paper and the authors regret any confusion and inconvenience this may have caused the readers of JBMR.