Abstract
Angiogenesis in the ovary facilitates oxygen, nutrient and hormone delivery. VEGF, which plays a key role in regulation of ovarian follicle development, is differentially spliced in the terminal exon to form two families of proteins, VEGFxxx (angiogenic) and VEGFxxxb (anti‐angiogenic). To identify the 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 mice. RT‐PCR and immunohistochemistry 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. The number of embryos released into oviducts by TG females were reduced to 82±6% of control mice. 38.5% of TG females had embryos lacked the Cumulus Cell‐Oocyte Complex, while none from WT females. Overexpression of VEGF165b appears to reduce fertility, possibly by its anti‐angiogenic actions on follicular development.Supported by the Wellcome Trust and British Heart Foundation.
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