The classical pink-eyed dilution mutation affects angiogenic responsiveness.

Angiogenesis is the process by which new blood vessels are formed from existing vessels. Mammalian populations, including humans and mice, harbor genetic variations that alter angiogenesis. Angiogenesis-regulating gene variants can result in increased susceptibility to multiple angiogenesis-dependent diseases in humans.

Endostatin inhibits the growth of endometriotic lesions but does not affect fertility.

Objective: To determine whether endometriosis can be treated with the angiogenesis inhibitor endostatin and the effect of this treatment on fertility and reproduction.

Design: Pharmacologic intervention in a surgically induced model of endometriosis and in female mice undergoing mating.

Setting: Animal research facility.

Nonsteroidal antiinflammatory drugs differentially suppress endometriosis in a murine model.

Objective: To determine whether nonsteroidal antiinflammatory drugs (NSAIDs) affect the establishment and progression of endometriotic lesions in a murine model.

Design: Pharmacologic intervention in a surgically induced murine model of abdominal/peritoneal endometriosis.

Setting: Animal research facility.

Genetic loci that control the angiogenic response to basic fibroblast growth factor.

Angiogenesis is controlled by a balance between stimulatory growth factors and endogenous inhibitors. We propose that the balance of stimulators and inhibitors, as well as the general sensitivity of the endothelium to these factors, varies from individual to individual. Indeed, we have found that individual mouse strains have dramatically different responses to growth factor-induced neovascularization.

Genetic loci that control vascular endothelial growth factor-induced angiogenesis.

Angiogenesis is regulated by the balance between angiogenic stimulators and inhibitors. Numerous reports have demonstrated that tumors induce aggressive angiogenesis by up-regulating the production of angiogenesis stimulating growth factors to overcome the baseline levels of endogenous inhibitors. However, the possibility of large differences in the host's responsiveness to angiogenic factors has been largely overlooked.

Injection of antiangiogenic agents into the macaque preovulatory follicle: disruption of corpus luteum development and function.

Ovulation and conversion of the follicle into the corpus luteum involve remarkable changes in vascular permeability and neovascularization of the luteinizing granulosa layer. To evaluate the importance of these vascular events in follicle rupture and luteal development, sequential experiments were designed in which vehicle or angiogenic inhibitors (TNP-470 or angiostatin) were injected directly into the preovulatory follicle of rhesus monkeys during spontaneous menstrual cycles. After control injections, 13 of 14 animals exhibited serum levels of progesterone (P) during the subsequent luteal phase that were comparable to untreated animals in our colony.