High-cell density-induced VCAM1 expression inhibits the migratory ability of mesenchymal stem cells

Cell Biol Int. 2011 May;35(5):475-81. doi: 10.1042/CBI20100372.


MSCs (mesenchymal stem cells) migrate into damaged tissue and then proliferate and differentiate into various cell lineages to regenerate bone, cartilage, fat and muscle. Cell-cell adhesion of MSCs is essential for the MSC-dependent tissue regeneration after their homing into a damaged tissue. However, it remains to be elucidated what kinds of adhesion molecules play important roles in the cell-cell communication between MSCs. In order to identify adhesion molecules that facilitate mutual contact between MSCs, a comprehensive analysis of mRNA expression in adhesion molecules was performed by comparing profiles of expression status of adhesion molecules in MSCs at low- and high-cell density. We found that the expression level of VCAM1 (vascular cell adhesion molecule-1)/CD106 was clearly up-regulated in the human bone marrow-derived MSCs-UE7T-13 cells - under a condition of high cell density. Intriguingly, the migratory ability of the cells was clearly accelerated by a knockdown of VCAM1. Furthermore, the migratory ability of UE7T-13 cells was decreased by the over expression of exogenous VCAM1. In addition, the high cell density-induced expression of VCAM1 was clearly suppressed by NF-κB (nuclear factor-κB) signalling-related protein kinase inhibitors such as an IKK-2 (IκB kinase-2) inhibitor VI. In conclusion, the high cell density-induced VCAM1 expression through the NF-κB pathway inhibits the migratory ability of human bone marrow-derived MSCs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Adhesion
  • Cell Count
  • Cell Line
  • Cell Movement*
  • Gene Expression Regulation / drug effects
  • Humans
  • Mesenchymal Stem Cells / cytology*
  • Mesenchymal Stem Cells / metabolism
  • NF-kappa B / metabolism
  • Protein Kinase Inhibitors / pharmacology
  • RNA, Messenger / genetics
  • Vascular Cell Adhesion Molecule-1 / genetics*
  • Vascular Cell Adhesion Molecule-1 / metabolism


  • NF-kappa B
  • Protein Kinase Inhibitors
  • RNA, Messenger
  • Vascular Cell Adhesion Molecule-1