Abstract
Pathological angiogenesis contributes to diseases as varied as cancer and corneal neovascularization. The vascular endothelial growth factor (VEGF) - VEGF receptor 2 (KDR/VEGFR2) axis has been the major target for treating pathological angiogenesis. However, VEGF-targeted therapies exhibit reduced efficacy over time, indicating that new therapeutic strategies are needed. Therefore, identifying new targets that mediate angiogenesis is of great importance. Here, we report that one of the anthrax toxin receptors, capillary morphogenesis gene 2 (ANTXR2/CMG2), plays an important role in mediating angiogenesis induced by both bFGF and VEGF. Inhibiting physiological ligand binding to CMG2 results in significant reduction of corneal neovascularization, endothelial tube formation and cell migration. We also report the novel finding that CMG2 mediates angiogenesis by regulating the direction of endothelial chemotactic migration without affecting overall cell motility.
Footnotes
changed figure legend on Figure S3. Assays on figure S3 were done in HMVECs not EAhy926 cells. Also changed figure 3, and S5. removed migration data with insulin and boiled FBS