Identification of brain-derived neurotrophic factor as a novel angiogenic protein in multiple myeloma.

摘要: Patients with multiple myeloma (MM) have increased bone marrow angiogenesis, but the angiogenic properties of cells and mechanism MM-induced angiogenesis not been completely clarified. The brain-derived neurotrophic factor (BDNF) its high-affinity receptor, TrkB, identified as critical factors in regulation vessel formation. In this study, we demonstrate that patients MM had BDNF vascular endothelial growth (VEGF) their peripheral blood. We also found particular a decreased level was correlated remission MM. expressed by human cell line RPMI8226 primary cells, TrkB umbilical vein (HUVEC) at protein levels. coculture system, observed both induced migration formation net-like structure HUVEC. anti-BDNF monoclonal antibody significantly partially restrained effect cells. Moreover, an experimental model vivo, VEGF promoted Matrigel plug compared to control. These effects were blocked antibody. Finally, our vitro results supported vivo finding xenograft NOD/SCID models. Anti-BDNF mAb treatment resulted inhibition tumor growth, density, necrosis. Our study suggested BDNF/TrkB signaling pathway could be involved, least part, angiogenesis.