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Deletion of cavin genes reveals tissue-specific mechanisms for morphogenesis of endothelial caveolae

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  • Carsten Gram Hansen

    (MRC Laboratory of Molecular Biology
    Present address: Sanford Consortium for Regenerative Medicine and UCSD, 2880 Torrey Pines Scenic Drive, La Jolla, California 92037, USA)

  • Elena Shvets

    (MRC Laboratory of Molecular Biology)

  • Gillian Howard

    (MRC Laboratory of Molecular Biology)

  • Kirsi Riento

    (MRC Laboratory of Molecular Biology)

  • Benjamin James Nichols

    (MRC Laboratory of Molecular Biology)

Abstract

Caveolae are abundant in endothelial cells and are thought to have important roles in endothelial cell biology. The cavin proteins are key components of caveolae, and are expressed at varied amounts in different tissues. Here we use knockout mice to determine the roles of cavins 2 and 3 in caveolar morphogenesis in vivo. Deletion of cavin 2 causes loss of endothelial caveolae in lung and adipose tissue, but has no effect on the abundance of endothelial caveolae in heart and other tissues. Changes in the morphology of endothelium in cavin 2 null mice correlate with changes in caveolar abundance. Cavin 3 is not required for making caveolae in the tissues examined. Cavin 2 determines the size of cavin complexes, and acts to shape caveolae. Cavin 1, however, is essential for normal oligomerization of caveolin 1. Our data reveal that endothelial caveolae are heterogeneous, and identify cavin 2 as a determinant of this heterogeneity.

Suggested Citation

  • Carsten Gram Hansen & Elena Shvets & Gillian Howard & Kirsi Riento & Benjamin James Nichols, 2013. "Deletion of cavin genes reveals tissue-specific mechanisms for morphogenesis of endothelial caveolae," Nature Communications, Nature, vol. 4(1), pages 1-13, June.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2808
    DOI: 10.1038/ncomms2808
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