The cellular mechanisms of angiogenesis involve motility and alignment of ECs to form a capillary tube-like network on matrigel [31].
Firstly, the ability of ECs to form tubes was assessed when grown in Matrigel.
This is replicated in vivo where dominant-negative N19RhoA impairs vessel assembly and dominant-active V14RhoA stimulates ECs to form vessels [ 89].
In fact, the composition of the ECM affects the ability of ECs to form networks (Dye et al. 2004) and sprouts (Kaijzel et al. 2006) in vitro.
However, GF-reduced Matrigel does itself act as a stimulant/activator inducing ECs to form tubules in the absence of exogenous GFs.
Nevertheless, investigations into the molecular interactions of these cell types in co-culture are crucial because both, ASCs and BMSCs, stimulate ECs to form vessel-like structures in vitro.
We identified a 20-amino-acid peptide derived from the β chain of FgnE, β43 63, which had no effect on EC proliferation or migration but markedly inhibited the ability of activated ECs to form tubules or to adhere to various constituents of the extracellular matrix – collagen IV, fibronectin and vitronectin.
Recently, different authors have shown that bone marrow-derived MSCs express pericyte markers and cooperate with ECs to form a vascular network in three-dimensional cultures, suggesting that these cells may derive from the bone marrow perivascular sites where they probably act as pericytes [ 24, 25].
Using an agent-based model, it was proposed that these rules allow ECs to form coherent tracks of cells navigating toward a VEGF-producing tumor, in a mechanism closely resembling one proposed previously for the formation of pheromone-mediated army ant raid patterns (Deneubourg et al. 1989).
This result agreed with the proliferation assay, since the ability of ECs to form tube-like structures is partly related to cell proliferation.
