Bone marrow cells recruited through the neuropilin-1 receptor promote arterial formation at the sites of adult neoangiogenesis in mice
J. Clin. Invest. Serena Zacchigna, et al. 118:2062 doi:10.1172/JCI32832 [Go to this article.]

Figure 6
A model to explain the role of BM cells in arteriogenesis. Artery formation relies on the occurrence of 2 concomitant events, namely the activation of the local endothelium (through the canonical VEGF receptors) and the recruitment of BM-derived mononuclear cells through the NP-1 receptor; these cells in turn engage SMCs to the sites of endothelial activation. Only VEGF₁₆₅ is able to stimulate both events and is thus arteriogenic. In contrast, VEGF₁₂₁ activates the endothelium locally, thus inducing capillary sprouting, but is not able to bind NP-1, and thus it does not recruit BM cells nor does it form arteries. Finally, Sema3A, a high-affinity ligand for NP-1, is a potent recruiter of mononuclear cells from the BM, but it exerts an inhibitory effect on endothelial cells and therefore is not angiogenic.