Increased expression of vascular endothelial growth factor in placentas of p57Kip2 null embryos

FEBS Letters

Takahashi, Katsuhiko²  Tomita, Motowo²  Kobayashi, Takao³  Kanayama, Naohiro³  Nakayama, Keiko¹  Matsuura, Toshiki³  Choi-Miura, Nam-Ho² 

[1] Laboratory of Embryonic and Genetic Engineering, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan;Department of Physiological Chemistry, School of Pharmaceutical Sciences, Showa University 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan;Department of Obstetrics and Gynecology, Hamamatsu University School of Medicine 1-20-1 Handayama, Hamamatsu, Shizuoka 431-3192, Japan

关键词: p57Kip2;    Genomic imprinting;    Placentation;    Preeclampsia;    VEGF;    VEGF;    vascular endothelial growth factor;    PlGF;    placenta growth factor;    PBS;    phosphate-buffered saline;    GAPDH;    glyceraldehyde-3-phosphate dehydrogenase;    mRNA;    messenger RNA;    PCR;    polymerase chain reaction;    RT;    reverse transcription;   

DOI  :  10.1016/S0014-5793(02)03681-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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 (PlGF). 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. PlGF 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.

【 授权许可】

Unknown