Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Correspondence
  • Published:

Lack of HIF-2α in limb bud mesenchyme causes a modest and transient delay of endochondral bone development

Nature Medicine volume 17, pages 25–26 (2011)Cite this article

Subjects

To the Editor:

Two papers recently published in Nature Medicine provide evidence that hypoxia-inducible factor-2α (HIF-2α) is crucial for articular surface homeostasis through mechanisms that involve, at least in part, regulation of genes such as Col10a1 (encoding the α1 chain of type X collagen, Col10A1), Mmp13 (encoding matrix metalloproteinase-13, MMP-13) and Vegfa (encoding vascular endothelial growth factor-A, VEGF)1,2. Interestingly, Saito et al.1 also report a mild delay of chondrocyte hypertrophy in fetal growth plates of mice heterozygous for genetic knockout of HIF-2α (encoded by Epas1). The key implication of this finding is that homozygous loss of HIF-2α would markedly delay chondrocyte hypertrophy and replacement of cartilage by bone. However, as shown below, we found that this was not the case.

This is a preview of subscription content, access via your institution

Relevant articles

Open Access articles citing this article.

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Phenotypical analysis of Prx1-Cre; Epas1fl/fl and control littermates in embryonic and neonatal stages.

References

  1. Saito, T. et al. Nat. Med. 16, 678–686 (2010).

    Article  CAS  Google Scholar 

  2. Yang, S. et al. Nat. Med. 16, 687–693 (2010).

    Article  CAS  Google Scholar 

  3. Gordon, J.D. & Simon, M. Curr. Opin. Genet. Dev. 17, 71–77 (2007).

    Article  Google Scholar 

  4. Araldi, E. & Schipani, E. Bone 47, 190–196 (2010).

    Article  CAS  Google Scholar 

  5. Provot, S. et al. J. Cell Biol. 177, 451–464 (2007).

    Article  CAS  Google Scholar 

Download references

Acknowledgements

This paper was supported by US National Institutes of Health grant RO1 AR048191-06 to E.S.

Author information

Authors and Affiliations

  1. Department of Medicine, Endocrine Unit, Massachusetts General Hospital–Harvard Medical School, Boston, Massachusetts, USA

    Elisa Araldi, Richa Khatri & Ernestina Schipani

  2. Division of Cancer and Radiation Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, USA

    Amato J Giaccia

  3. Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA

    M Celeste Simon

Authors
  1. Elisa Araldi
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Richa Khatri
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Amato J Giaccia
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. M Celeste Simon
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Ernestina Schipani
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Ernestina Schipani.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Supplementary information

Supplementary Text and Figures

Supplementary Fig. 1 and Supplementary Methods (PDF 3159 kb)

Rights and permissions

Reprints and permissions

About this article

Cite this article

Araldi, E., Khatri, R., Giaccia, A. et al. Lack of HIF-2α in limb bud mesenchyme causes a modest and transient delay of endochondral bone development. Nat Med 17, 25–26 (2011). https://doi.org/10.1038/nm0111-25

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nm0111-25

This article is cited by

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing