Activation of the canonical Wnt/beta-catenin pathway enhances monocyte adhesion to endothelial cells

Biochem Biophys Res Commun. 2006 Aug 18;347(1):109-16. doi: 10.1016/j.bbrc.2006.06.082. Epub 2006 Jun 22.

Abstract

Monocyte adhesion to vascular endothelium has been reported to be one of the early processes in the development of atherosclerosis. In an attempt to develop strategies to prevent or delay atherosclerosis progression, we analyzed effects of the Wnt/beta-catenin signaling pathway on monocyte adhesion to various human endothelial cells. Adhesion of fluorescein-labeled monocytes to various human endothelial cells was analyzed under a fluorescent microscope. Unlike sodium chloride, lithium chloride enhanced monocyte adhesion to endothelial cells in a dose-dependent manner. We further demonstrated that inhibitors for glycogen synthase kinase (GSK)-3beta or proteosome enhanced monocyte-endothelial cell adhesion. Results of semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) indicated that activation of Wnt/beta-catenin pathway did not change expression levels of mRNA for adhesion molecules. In conclusion, the canonical Wnt/beta-catenin pathway enhanced monocyte-endothelial cell adhesion without changing expression levels of adhesion molecules.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Adhesion / drug effects
  • Cell Adhesion / physiology*
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects
  • Endothelial Cells / physiology*
  • Humans
  • Lithium / administration & dosage
  • Monocytes / cytology
  • Monocytes / drug effects
  • Monocytes / physiology*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*
  • Wnt Proteins / metabolism*
  • beta Catenin / metabolism*

Substances

  • CTNNB1 protein, human
  • Wnt Proteins
  • beta Catenin
  • Lithium