Proliferation hemangiomas formation through dual mechanism of vascular endothelial growth factor mediated endothelial progenitor cells proliferation and mobilization through matrix metalloproteinases 9.

Summary Infantile hemangioma is the most common tumor of infancy and the mechanism leading to proliferation hemangiomas formation is poorly understood and currently no successful treatment modality exists. We hypothesize that EPCs formed during proliferation hemangiomas, as the result of vascular endothelial growth factor (VEGF) stimulation through MMP9, play the major role in the control of cell proliferation and capillary-like vessels production. Accepting the hypothesis to be correct, a therapy that inhibits EPC mobilization and proliferation can be used to prevent the proliferation hemangiomas formation. Current therapies are only partially effective and safe because they could not eliminate all the relative factors of proliferation hemangiomas formation at all, such as: EPCs in the peripheral blood, and at the same time inducing death (apoptosis and necrosis) of other normal cells. A more efficient prevention of proliferation hemangiomas could be achieved using specific drugs or biologic methods that inhibit EPC mobilization and proliferation. Therapy based on gene therapy, capable to specifically inhibit VEGF and MMP9 expression in gene level, can be possibly effective.