Placentas of mice lacking p57Kip2 expression have trophoblastic hyperplasia. To elucidate the mechanism underlying this phenomenon, we studied expression of two angiogenic factors, vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF). Immunohistochemical analysis with anti-VEGF antibodies indicated that VEGF expression was stronger and more clearly detectable in placentas of p57Kip2 null embryos compared to wild-type placentas. PlGF showed no significant differences between placentas of p57Kip2 null and wild-type embryos. In quantitative analysis, placentas of p57Kip2 null embryos showed higher VEGF messenger (m)RNA and protein levels than did wild-type placentas. PlGF mRNA and protein levels were not significantly different. These findings suggest that VEGF is involved in the hyperplasia that occurs in placentas of p57Kip2 null embryos.
- Genomic imprinting