Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10891432 | Stem Cell Research | 2011 | 13 Pages |
Abstract
Mechanisms underlying the vascular differentiation of human bone marrow stromal cells (HBMSCs) and their contribution to neovascularisation are poorly understood. We report the essential role of cell density-induced signals in directing HBMSCs along endothelial or smooth muscle lineages. Plating HBMSCs at high density rapidly induced Notch signaling, which initiated HBMSC commitment to a vascular progenitor cell population expressing markers for both vascular lineages. Notch also induced VEGF-A, which inhibited vascular smooth muscle commitment while consolidating differentiation to endothelial cells with cobblestone morphology and characteristic endothelial markers and functions. These mechanisms can be exploited therapeutically to regulate HBMSCs during neovascularisation.
Keywords
vWFαSMAHES-1PECAM-1VCAM-1VSMCN-[N-(3,5-difluorophenacetyl-L-alanyl)]-S-phenylglycine t-butyl esterhBMSCsDAPTHUVECSVEGFR1Smooth Muscle Alpha ActinDMSOECsVE-cadherinEDTAEthylenediaminetetraacetic acidDimethyl sulfoxideVascular smooth muscle cellHuman bone marrow stromal cellsHuman umbilical vein endothelial cellsEndothelial cellsvon Willebrand factor.Vascular endothelial growth factorVascular Endothelial Growth Factor (VEGF)low density lipoproteinLDLvascular cell adhesion moleculevascular endothelial cadherinvascular endothelial growth factor receptor 1
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Authors
Jemima L. Whyte, Stephen G. Ball, C. Adrian Shuttleworth, Keith Brennan, Cay M. Kielty,