ADAM9 is present at endothelial cell - cell junctions and regulates monocyte - endothelial transmigration

Biochem Biophys Res Commun. 2017 Nov 18;493(2):1057-1062. doi: 10.1016/j.bbrc.2017.09.089. Epub 2017 Sep 18.

Abstract

We have found that A Disintegrin And Metalloproteinase-9 (ADAM9) localises to cell-cell junctions with VE-Cadherin in confluent endothelial monolayers. Co-cultures of cells separately transfected with ADAM9-EGFP or ADAM9-HA showed expression is required in two adjacent cells for localisation to cell-cell junctions suggesting the ADAM9 ectodomain may self-associate. A direct interaction between ADAM9 ectodomains was confirmed using recombinant proteins and an ELISA based method. As the ADAM9 ectodomain can also exist as a soluble form physiologically, we examined if this could inhibit endothelial functions dependent on cell-cell junctions. The soluble ADAM9 ectodomain could not increase endothelial monolayer permeability or inhibit monocyte-endothelial adhesion, but could inhibit monocyte-endothelial transmigration. These novel findings point to ADAM9 playing an important role in endothelial cell biology that is distinct from the other ADAMs.

Keywords: ADAM9; Endothelial; Monocyte; Permeability; Transmigration; VE-Cadherin.

MeSH terms

  • ADAM Proteins / analysis
  • ADAM Proteins / metabolism*
  • Animals
  • Cell Line
  • Endothelial Cells / cytology*
  • Endothelial Cells / metabolism
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Intercellular Junctions / metabolism*
  • Intercellular Junctions / ultrastructure
  • Membrane Proteins / analysis
  • Membrane Proteins / metabolism*
  • Mice
  • Monocytes / cytology*
  • Monocytes / metabolism
  • Protein Domains
  • Transendothelial and Transepithelial Migration*

Substances

  • Membrane Proteins
  • ADAM Proteins
  • ADAM9 protein, human
  • Adam9 protein, mouse