title: Molecular mechanisms of developmental and tumor angiogenesis.
abstract: Angiogenesis, the sprouting of capillaries from preexisting vessels, is of fundamental importance during embryonic development and is the principal process by which the brain and certain other organs become vascularized. Angiogenesis occurs during embryonic development but is almost absent in adult tissues. Transient and tightly controlled (physiological) angiogenesis in adult tissues occurs during the female reproductive cycle and during wound healing. In contrast, pathological angiogenesis is characterized by the persistent proliferation of endothelial cells, and is a prominent feature of diseases such as proliferative retinopathy, rheumathoid arthritis, and psoriasis. In addition, many tumors are able to attract blood vessels from neighbouring tissues. Tumor-induced angiogenesis requires a constitutive activation of endothelial cells. These endothelial cells dissolve their surrounding extracellular matrix, migrate toward the tumor, proliferate, and form a new vascular network, thus supplying the tumor with nutrients and oxygen and removing waste products. The onset of angiogenesis in human gliomas is characterized by the expression of genes encoding angiogenic growth factors such as vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF) in tumor cells, and coordinate induction of genes in endothelial cells which encode the respective growth factor receptors. Developmental and tumor angiogenesis appear to be regulated by a paracrine mechanism involving VEGF and VEGF receptor-1 and -2.
authors.affiliation: Abteilung Neuropathologie, Klinikum der Philipps-Universität, Marburg, Germany.
authors.forename: K H
authors.initials: KH
authors.lastname: Plate
authors.forename: G
authors.initials: G
authors.lastname: Breier
authors.forename: W
authors.initials: W
authors.lastname: Risau
mesh_terms: D000818:Animals; D001921:Brain / Q000098:blood supply* / Q000254:growth & development; D001932:Brain Neoplasms / Q000098:blood supply* / Q000473:pathology; D002196:Capillaries / Q000502:physiology / Q000503:physiopathology; D002455:Cell Division; D005314:Embryonic and Fetal Development; D016228:Endothelial Growth Factors / Q000096:biosynthesis; D004730:Endothelium, Vascular / Q000166:cytology / Q000473:pathology; D005260:Female; D005909:Glioblastoma / Q000098:blood supply / Q000473:pathology; D006801:Humans; D008222:Lymphokines / Q000096:biosynthesis; D009369:Neoplasms / Q000098:blood supply* / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000473:pathology / Q000503:physiopathology*; D010982:Platelet-Derived Growth Factor / Q000096:biosynthesis; D020794:Receptor Protein-Tyrosine Kinases / Q000502:physiology; D017978:Receptors, Growth Factor / Q000502:physiology; D040262:Receptors, Vascular Endothelial Growth Factor; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D014945:Wound Healing
chemical_list: D016228:Endothelial Growth Factors; D008222:Lymphokines; D010982:Platelet-Derived Growth Factor; D017978:Receptors, Growth Factor; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D020794:Receptor Protein-Tyrosine Kinases; D040262:Receptors, Vascular Endothelial Growth Factor