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Recent evidence points to the involvement of vascular endothelial growth factor (VEGF) in mammalian reproductive physiology. Transgenic mice expressing VEGF (121 isoform) under the control of the polyepithelial mucin-1 (muc-1) promoter showed a reduction in male fertility due to impaired spermiogenesis, and aberrant placentation leading to preferential rejection of male embryos. A skew in the sex ratio of the litters was seen (three females to two males), independently of whether the transgene was carried by the male or female parent. In-situ hybridization permitted distinction of expression of the human VEGF transgene from endogenous mouse VEGF, and confirmed expression of the transgene in a wide range of epithelial tissues. Expression of the transgene in spermatocytes and in the embryonic portion of placenta is thought to be responsible for the reduced fertility and embryonic resorptions respectively. Males showed either complete sperm maturation arrest or various gradations of partial fertility. Abnormally high or low VEGF in human semen has been reported to be correlated with a lack of pregnancy success following IVF. The muc1-VEGF (121 isoform) transgenic mouse provides an animal model with which to further study this VEGF-induced pathology.

Type

Journal article

Journal

Mol hum reprod

Publication Date

03/2001

Volume

7

Pages

255 - 264

Keywords

Animals, Endothelial Growth Factors, Enzyme-Linked Immunosorbent Assay, Female, Fertility, Gene Expression, Humans, In Situ Hybridization, In Situ Nick-End Labeling, Kidney, Lymphokines, Male, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Transgenic, Microscopy, Electron, Mucins, Placenta, Promoter Regions, Genetic, Proto-Oncogene Proteins, Receptor Protein-Tyrosine Kinases, Receptors, Growth Factor, Receptors, Vascular Endothelial Growth Factor, Testis, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factor Receptor-1, Vascular Endothelial Growth Factors