Vascular endothelial growth factor transgenic mice exhibit reduced male fertility and placental rejection
- Resource Type
- Authors
- R. Poulsom; Roy Bicknell; S. Lui; Lukasz Huminiecki; H.Y. Chan; G. Stamp; A. L. Harris
- Source
- Molecular Human Reproduction. 7:255-264
- Subject
- Male
Vascular Endothelial Growth Factor A
Embryology
Placenta
Gene Expression
Endothelial Growth Factors
Testicle
Kidney
Mice
chemistry.chemical_compound
Testis
Promoter Regions, Genetic
In Situ Hybridization
Lymphokines
Vascular Endothelial Growth Factors
Obstetrics and Gynecology
Embryo
Vascular endothelial growth factor
medicine.anatomical_structure
Female
Genetically modified mouse
medicine.medical_specialty
Transgene
Enzyme-Linked Immunosorbent Assay
Mice, Transgenic
Biology
Proto-Oncogene Proteins
Internal medicine
In Situ Nick-End Labeling
Genetics
medicine
Animals
Humans
Receptors, Growth Factor
Molecular Biology
Vascular Endothelial Growth Factor Receptor-1
Mucins
Receptor Protein-Tyrosine Kinases
Placentation
Cell Biology
Sperm
Mice, Inbred C57BL
Microscopy, Electron
Fertility
Receptors, Vascular Endothelial Growth Factor
Endocrinology
Reproductive Medicine
chemistry
Mice, Inbred CBA
Developmental Biology
- Language
- ISSN
- 1460-2407
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.