Regulation of endothelial cell adherens junctions by a Ras-dependent signal transduction pathway

Biochem Biophys Res Commun. 1999 Jul 5;260(2):371-6. doi: 10.1006/bbrc.1999.0919.

Abstract

Adherens junctions, consisting of transmembrane cadherin molecules and their associated cytoplasmic alpha-, beta-, and gamma-catenin proteins, are thought to be critical for the development of stable cell adhesion and subsequent 3-dimensional tissue organization. In human endothelial cells there is a marked induction of gamma-catenin levels when cells reach confluence. We demonstrate that expression of a dominant negative ras gene product (N17ras) via adenoviral mediated gene transfer inhibits the confluent-dependent rise in gamma-catenin mRNA and protein levels. Consistent with its effects on overall gamma-catenin levels, expression of N17ras also reduces the amount of gamma-catenin associated with the adherens junction. Finally, although expression of N17ras under normal culture conditions produces no clear morphological phenotype, endothelial cells expressing a dominant negative ras gene product fail to form 3-dimensional, vascular-like structures when plated on reconstituted extracellular matrix.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviridae / genetics
  • Cell Adhesion*
  • Cells, Cultured
  • Cytoskeletal Proteins / genetics
  • Cytoskeletal Proteins / metabolism
  • Desmoplakins
  • Endothelium, Vascular / cytology*
  • Fluorescent Antibody Technique, Indirect
  • Gap Junctions / metabolism*
  • Humans
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Signal Transduction*
  • gamma Catenin
  • ras Proteins / metabolism*

Substances

  • Cytoskeletal Proteins
  • Desmoplakins
  • JUP protein, human
  • RNA, Messenger
  • gamma Catenin
  • ras Proteins