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PPAR-γ regulates pharmacological but not physiological or pathological osteoclast formation

Nature Medicine volume 22, pages 1203–1205 (2016)Cite this article

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The formation of LysM KO bone-resorptive cells in vitro mirrors that of their control counterparts, which indicates that PPAR-γ does not regulate basal osteoclastogenesis (Fig. 1b). To determine whether the same holds true in vivo, we histomorphometrically quantitated the tibiae of control mice and mice with conditional genetic deletions. We find that trabecular bone volume and the abundance of osteoclasts, whether expressed as the number per mm of trabecular bone surface or as the percentage of trabecular surface bearing tartrate-resistant acid phosphatase (TRAP)-expressing cells, are the same in both genotypes (Fig. 1c). We next subjected LysM KO and Cont mice to skeletal micro-computed tomography (μCT) analysis. In support of histomorphometry, trabecular bone volume and the parameters of cancellous architecture are similar in both groups (Fig. 1d).

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Figure 1: PPAR-γ deficiency does not affect physiological osteoclast differentiation in vitro and in vivo.

References

  1. Grey, A. Diabetes Obes. Metab. 11, 275–284 (2009).

    Article  CAS  Google Scholar 

  2. Wan, Y., Chong, L.W. & Evans, R.M. Nat. Med. 13, 1496–1503 (2007).

    Article  CAS  Google Scholar 

  3. Fukunaga, T., Zou, W., Rohatgi, N., Colca, J.R. & Teitelbaum, S.L. J. Bone Miner. Res. 30, 481–488 (2015).

    Article  Google Scholar 

  4. Korganow, A.S. et al. Immunity 10, 451–461 (1999).

    Article  CAS  Google Scholar 

  5. Clausen, B.E., Burkhardt, C., Reith, W., Renkawitz, R. & Förster, I. Transgenic Res. 8, 265–277 (1999).

    Article  CAS  Google Scholar 

  6. Maeda, K. et al. Nat. Med. 18, 405–412 (2012).

    Article  CAS  Google Scholar 

  7. de Boer, J. et al. Eur. J. Immunol. 33, 314–325 (2003).

    Article  CAS  Google Scholar 

  8. McCommis, K.S. et al. Cell Metab. 22, 682–694 (2015).

    Article  CAS  Google Scholar 

  9. Chen, Z. et al. J. Biol. Chem. 287, 23537–23548 (2012).

    Article  CAS  Google Scholar 

  10. Wei, W. et al. Mol. Cell. Biol. 31, 4692–4705 (2011).

    Article  CAS  Google Scholar 

  11. Izawa, T. et al. Cell Rep. 11, 1625–1637 (2015).

    Article  CAS  Google Scholar 

  12. Lam, J. et al. J. Clin. Invest. 106, 1481–1488 (2000).

    Article  CAS  Google Scholar 

Download references

Acknowledgements

This work was supported by US National Institutes of Health grants R37 AR046523 (S.L.T.), P30 AR057235 (S.L.T.), R01 AR54326 (Y.A.), R01 AR49192 (Y.A.) and P30 DK020579 (J.S.); and by Shriners Hospitals for Children grant 85400-STL (S.L.T.). RANK-Cre mice were generously provided by N. Takahashi (Matsumoto Dental University, Japan). Tie2original knockout mice were generously provided by Y. Wan (University of Texas).

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Authors and Affiliations

  1. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA

    Wei Zou, Nidhi Rohatgi & Steven L Teitelbaum

  2. Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, Missouri, USA

    Timothy Hung-Po Chen & Yousef Abu-Amer

  3. Department of Medicine, Division of Cardiology, Washington University School of Medicine, St. Louis, Missouri, USA

    Joel Schilling

  4. Department of Medicine, Division of Bone and Mineral Diseases, Washington University School of Medicine, St. Louis, Missouri, USA

    Steven L Teitelbaum

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  1. Wei Zou
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  2. Nidhi Rohatgi
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Correspondence to Steven L Teitelbaum.

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Zou, W., Rohatgi, N., Chen, TP. et al. PPAR-γ regulates pharmacological but not physiological or pathological osteoclast formation. Nat Med 22, 1203–1205 (2016). https://doi.org/10.1038/nm.4208

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