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Endothelial tubulogenesis is a complex process that requires multiple endothelial cell functions, including proliferation, migration, invasion and differentiation [16].
The results identified the growth factors, receptors and transcription factors expressed by these multiple endothelial cell types.
The results provide a comprehensive and quantitative analysis of gene use in these multiple endothelial cell populations.
In vivo studies also indicated that netrins promoted neovascularization and reperfusion in a murine model of peripheral vascular disease and also induced migration, proliferation and tube formation during in vitro studies involving multiple endothelial cell lines [24].
Endothelial cells that comprise tumour blood vessels have poor organization, leading to gaps between cells, multiple endothelial cell layers, and unusual tortuosity and branching [ 8, 9].
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Confocal microscopy analysis shows that vSMC extend filopodia that co-localize with multiple endothelial cells at various points both above and below the focal plane (Figure 2D).
Blood vascular islands often contained multiple endothelial cells.
These models show that epithelial endothelial binding occurs rapidly and that trans-endothelial migration is initiated at the intercellular joints between multiple endothelial cells.
However, since pre-eclampsia affects a variety of vascular beds, it is likely that characteristics common to multiple different endothelial cell types are important.
Angiogenesis consists of multiple steps including endothelial cell proliferation, migration, invasion and tube formation.
These incongruous results might be explained by the existence of multiple factors directing endothelial cell migration, including initial tumour size, extent of vascularity, differences in detection time after cell injection, total number of injected cells, and differences in the microenvironment of marrow-derived cells vs BOECs in vivo.
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