@entity172 promotes angiogenic activity in XXXX umbilical vein endothelial cells in vitro and in a @entity19 model.

@entity1 @entity172 @entity66 @entity5 @entity19 @entity53 @entity230 @entity1299
BACKGROUND: Angiogenesis is a critical event in wound healing, @entity5 growth, and the inflammatory vasculitides. Since @entity1 have a higher incidence of many @entity66 , we examined the effects of female sex @entity230 , particularly @entity53 , on @entity1 umbilical vein endothelial cell (HUVEC) behavior in vitro and on angiogenesis in vivo. METHODS AND RESULTS: HUVECs were grown in @entity172 -free medium before each assay. Exogenous @entity53 (1 to 5 nmol/L) increased cell attachment to laminin, types I and IV collagen, and fibronectin, as well as to tissue culture plastic. After a confluent monolayer of cells was "wounded" by scraping, @entity53 -treated (10(-8) mol/L) cells migrated into the wound three times faster than untreated cells. Cell proliferation on plastic and on laminin increased threefold to fivefold, respectively, in the presence of @entity53 . @entity53 also enhanced the ability of HUVECs to organize into tubular networks when plated on a reconstituted basement membrane, Matrigel. @entity53 effects on both the "wounding" assay and tube formation were blocked by the specific @entity172 receptor antagonist @entity1299 . Ovariectomy markedly decreased in vivo vascularization of Matrigel plugs coinjected with basic fibroblast growth factor in @entity19 . With @entity172 replacement, angiogenesis was increased to the levels observed in nonovariectomized @entity19 . CONCLUSIONS: These studies demonstrate that, in vitro and in vivo, @entity53 enhances endothelial cell activities important in neovascularization and suggest a promoting influence of estrogens on angiogenesis.
