Journal
FEBS LETTERS
Volume 532, Issue 3, Pages 283-288Publisher
WILEY
DOI: 10.1016/S0014-5793(02)03681-5
Keywords
p57(Kip2); genomic imprinting; placentation; preeclampsia; VEGF
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Placentas of mice lacking p57(Kip2) 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 (PIGF). Immunohistochemical analysis with anti-VEGF antibodies indicated that VEGF expression was stronger and more clearly detectable in placentas of p57(Kip2) null embryos compared to wild-type placentas. PIGF showed no significant differences between placentas of p57(Kip2) null and wild-type embryos. In quantitative analysis, placentas of p57(Kip2) 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 p57(Kip2) null embryos. (C) 2002 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.
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