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

Carsten Gram Hansen, Elena Shvets, Gillian Howard, Kirsi Riento, Benjamin James Nichols

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Pages (from-to)1831
JournalNature Communications
Volume4
DOIs
Publication statusPublished - 2013

Keywords

  • Animals
  • Caveolae
  • Caveolin 1
  • Cell Shape
  • Endothelial Cells
  • Endothelium
  • Gene Deletion
  • Lung
  • Membrane Proteins
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Molecular Weight
  • Morphogenesis
  • Multiprotein Complexes
  • Myocardium
  • Organ Specificity
  • Protein Structure, Quaternary
  • RNA-Binding Proteins

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