Apoptotic endothelial cells demonstrate increased adhesiveness for human mesenchymal stem cells
Article first published online: 20 NOV 2008
Copyright © 2008 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 219, Issue 1, pages 23–30, April 2009
How to Cite
Potapova, I. A., Cohen, I. S. and Doronin, S. V. (2009), Apoptotic endothelial cells demonstrate increased adhesiveness for human mesenchymal stem cells. J. Cell. Physiol., 219: 23–30. doi: 10.1002/jcp.21645
- Issue published online: 20 JAN 2009
- Article first published online: 20 NOV 2008
- Manuscript Accepted: 20 OCT 2008
- Manuscript Received: 29 AUG 2008
- American Heart Association Scientist Development
- NIH. Grant Numbers: HL67101, HL28958
Mesenchymal stem cells (MSCs) participate in the wound healing process in mammalians. Adhesion of MSCs to endothelium is a key step in the homing of MSCs circulating in the bloodstream to the sites of injury and inflammation. Because endothelial cells (ECs) may become apoptotic under certain pro-inflammatory conditions, we investigated the effects of pro-inflammatory, TNF-α and IL-1β, and pro-apoptotic agents, actinomycin D, cycloheximide, okadaic acid, wortmannin, and staurosporine, on human MSCs (hMSCs) adhesion to ECs. Treatment of ECs with pro-apoptotic agents markedly increased adhesion of hMSCs to ECs. This adhesion correlated with reduction of mitochondrial membrane potential, inhibition of NADH dehydrogenases, and release of von Willebrand factor (vWF) by ECs. Treatment of ECs with exogenous vWF also stimulated hMSC adhesion. These data provide evidence that apoptosis of ECs may regulate homing of hMSCs to the sites of tissue injury. These results are consistent with the hypothesis that activation of apoptotic signaling pathways in ECs releases vWF which regulates hMSC adhesion to ECs. J. Cell. Physiol. 219: 23–30, 2009. © 2008 Wiley-Liss, Inc.