| Institution: | (1) Department of Anatomy, University Hospital Eppendorf, Hamburg, Germany;(2) Department of Urology, University Hospital Eppendorf, Hamburg, Germany;(3) Department of Clinical Chemistry, University Hospital Eppendorf, Hamburg, Germany;(4) Department of Hematology/Oncology, University Hospital Eppendorf, Hamburg, Germany;(5) Department of Neuropathology, University Hospital Eppendorf, Hamburg, Germany;(6) Department of Pharmacology, University Hospital Eppendorf, Hamburg, Germany;(7) Department of Pathology, University Hospital Eppendorf, Hamburg, Germany;(8) Department of Surgical Research, Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA |
| Abstract: | Endostatin decreased vascular endothelial growth factor (VEGF)-induced formation of endothelial tubes and microvessels sprouting
from aortic rings and blocked their network. After cessation of treatment, the survival time of endostatin plus VEGF-treated
tubes was approximately doubled in comparison to VEGF alone. Endostatin antibody blocked VEGF-induced endothelial tube formation
and disrupted existing tubes. Endostatin immunostaining was localized between endothelium and basement membrane and in inter-endothelial
junctions of new, but not of quiescent, blood vessels. In tumors grown in SCID mice, endostatin immunostaining was stronger
accompanying blood vessel maturation and was significantly prominent in vessels of tumor marginal zone where angiogenesis
is highly active. These data indicate a new antiangiogenic action of endostatin stabilizing and maturating endothelial tubes
of newly formed blood vessels. Thus, strategies accelerating vascular stabilization and maturation could be promising in tumor
therapy.
This revised version was published online in June 2006 with corrections to the Cover Date. |
