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Overexpression of VEGF165b in mouse ovary results in reduced litter size
Author(s) -
Qiu Yan,
Murphy David,
Harper Steven J.,
Bates David O.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.774.24
Subject(s) - litter , ovary , medicine , biology , endocrinology , angiogenesis , follicular phase , andrology , follicle , transgene , embryo , gene , microbiology and biotechnology , genetics , agronomy
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, VEGF xxx (angiogenic) and VEGF xxx b (anti‐angiogenic). To identify the function of VEGF 165 b in the ovary, nine female transgenic mice (TG) overexpressing VEGF 165 b 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 VEGF 165 b 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 VEGF 165 b appears to reduce fertility, possibly by its anti‐angiogenic actions on follicular development. Supported by the Wellcome Trust and British Heart Foundation.