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

Carsten Gram Hansen, Elena Shvets, Gillian Howard, Kirsi Riento and Benjamin James Nichols ()
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Carsten Gram Hansen: MRC Laboratory of Molecular Biology
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

Nature Communications, 2013, vol. 4, issue 1, 1-13

Abstract: 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.

Date: 2013
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2808

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DOI: 10.1038/ncomms2808

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