Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2024 Jan 10;6(1):141–152. doi: 10.1038/s42255-023-00948-y

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 4 — a, Schematic overview of experimental setup for metabolomics analysis during osteoclastogenesis. [¹³C₅/¹⁵N₂]glutamine tracer was added (black stars) from d0 to d3 (that is, early differentiation), or from d3 to d6 (that is, late differentiation). b, Ser and Gly labelling from [¹³C₅/¹⁵N₂]glutamine at different timepoints during osteoclast differentiation (n = 4; one-way ANOVA). Relevant MDVs are shown; n denotes specific labelling from nitrogen. c, Intracellular αKG levels in vehicle and AOA-treated osteoclasts, or in control and PSAT1-silenced (shPSAT1) osteoclasts (n = 4; unpaired, two-tailed Student’s t-test). An empty vector was used as shRNA control. d, Schematic overview of experimental setup. Osteoclasts were treated with AOA during the first 3 d, the last 3 d or during the entire experiment. e,f, TRAP staining (e) and quantification of TRAP⁺ MNCs (f) from wild-type mice treated with either vehicle or AOA (n = 4; one-way ANOVA). g,h, TRAP staining (g) and quantification of TRAP⁺ MNCs (h) after shRNA-mediated silencing of PSAT1 (n = 4 biologically independent samples; unpaired, two-tailed Student’s t-test). An empty vector was used as control. i, Phgdh, Csf1r, Tnfrsf11a (encoding RANK), Nfatc1 (AOA: P = 0.002; shPSAT1: P = 0.008), Myc, Calcr (AOA: P = 0.006; shPSAT1: P = 0.013), Acp5 (AOA: P = 0.03; shPSAT1: P = 0.007), Ctsk (AOA: P < 0.0001; shPSAT1: P = 0.048), Dcstamp (AOA: P = 0.0095; shPSAT1: P = 0.013), Atp6v0d2 (AOA: P = 0.04; shPSAT1: P = 0.011), Mmp9 (AOA: P = 0.005; shPSAT1: P = 0.04) and Irf8 mRNA levels in AOA-treated or PSAT1-silenced osteoclasts (n = 4; unpaired, two-tailed Student’s t-test with *P < 0.05 versus vehicle/control). j, Schematic overview of experimental setup. PSAT1-silenced osteoclasts were treated with cell-permeable αKG during the entire experiment. k,l, TRAP staining (k) and quantification of control and αKG-treated PSAT1-silenced TRAP⁺ MNCs (l) (n = 4 biologically independent samples; one-way ANOVA). Data are means ± s.d. Scale bars, 50 µm (e, g and k).

Source data