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. Author manuscript; available in PMC: 2020 Nov 5.
Published in final edited form as: Cell Metab. 2019 Sep 12;30(5):890–902.e8. doi: 10.1016/j.cmet.2019.08.012

Figure 3. Glutamate mediates the stressor-induced release of bioactive osteocalcin from osteoblasts.

Figure 3.

(A) Supernatant Ocn levels after 1-hour treatment of osteoblasts with indicated neurotransmitters. (B) Serum glutamate levels before and after TMT exposure. (C) Serum Ocn levels and rate of Ocn release before and after TMT stress in pegylated diphtheria toxin (PEG-DT)- or vehicle-injected Vglut2iDTR mice. (D) Immunofluorescence of femoral metaphysis of WT mice, Ob: osteoblast, N: glutamatergic neurite (scale: 5 μm). (E) Expression of glutamate transporters in osteoblasts. (F) Radiolabeled glutamate transport into Glast−/− and WT osteoblasts treated with vehicle or UCPH102. (G) Ocn levels in supernatants after 1-hour treatment with glutamate and UCPH102 of untreated or warfarin pre-treated mouse osteoblast cultures. (H) Supernatant Ocn levels 1 hour after treatment of Glast−/− and WT osteoblasts with glutamate. (I) Serum Ocn levels and rate of Ocn release in Glast−/− and WT mice before and after TMT exposure. (J) GGCX activity on Ocn in WT osteoblast lysates treated with glutamate. (K) Serum Ocn in WT mice expressing hM3Dq in the BLA after injection of CNO or vehicle. Mice are 3-month-old females. Values are mean ±SEM. nd, not detectible. ns, not significant; *, p<.05; **, p<.01; by Student’s t-test or one-way ANOVA with bonferroni post hoc test.