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

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. Howev...

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Veröffentlicht in:Cell biology international 2011-05, Vol.35 (5), p.475-481
Hauptverfasser: Nishihira, Soko, Okubo, Naoto, Takahashi, Noriko, Ishisaki, Akira, Sugiyama, Yoshiki, Chosa, Naoyuki
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container_issue 5
container_start_page 475
container_title Cell biology international
container_volume 35
creator Nishihira, Soko
Okubo, Naoto
Takahashi, Noriko
Ishisaki, Akira
Sugiyama, Yoshiki
Chosa, Naoyuki
description 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.
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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. 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subjects Cell Adhesion
Cell Count
cell density
Cell Line
Cell Movement
Gene Expression Regulation - drug effects
Humans
mesenchymal stem cell
Mesenchymal Stromal Cells - cytology
Mesenchymal Stromal Cells - metabolism
migration
NF-kappa B - metabolism
nuclear factor-κB pathway
Protein Kinase Inhibitors - pharmacology
RNA, Messenger - genetics
vascular cell adhesion molecule-1
Vascular Cell Adhesion Molecule-1 - genetics
Vascular Cell Adhesion Molecule-1 - metabolism
title High-cell density-induced VCAM1 expression inhibits the migratory ability of mesenchymal stem cells
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