Abstract
Physiological angiogenesis occurs in the ovary, and facilitates oxygen, nutrient, and hormone substrate delivery and transfer of synthesized hormones to targeted cells. VEGF plays a key role in the regulation of ovarian follicle development and corpus luteum formation and maintenance.VEGF is differentially spliced in the terminal exon to form two families of proteins, termed VEGFxxx and VEGFxxxb, where xxx denotes the amino acid number. VEGF165b inhibits VEGF165 induced endothelial cell proliferation, migration, vasodilatation and in vivo angiogenesis,To identify the biological function of VEGF165b in the ovary, nine female transgenic mice (TG) overexpressing VEGF165b under the control of the MMTV promoter and 10 wild type (WT) female littermates were mated with WT C57Bl6 mice. RT‐PCR indicated strong expression of VEGF165b in ovaries of TG females. TG mothers produced litters of half the size of WT dams (3.3±0.4 vs. 5.8±0.7 pups/litter), or TG males (6.1±0.7 pups/litter). There was no developmental defect identified in either the WT or TG pups from TG mothers suggesting subfertility due to defects in the female reproductive system. We have therefore shown that over‐expression of VEGF165b reduces fertility, possibly by its anti‐angiogenic actions on follicular development. This project is supported by the Wellcome Trust and British Heart Foundation.
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