Localization of VEGF and expression of its receptors flt and KDR in human placenta throughout pregnancy.

Localization of VEGF and expression of its receptors flt and KDR in human placenta throughout pregnancy.
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整个妊娠期间人胎盘中 VEGF 的定位及其受体 flt 和 KDR 的表达。

DOI:
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发表时间:
1996
期刊:
影响因子:
6.1
通讯作者:
D. Charnock
D. Charnock
中科院分区:
医学1区
文献类型:
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作者:
D. Clark;Stephen K. Smith;A. Sharkey;D. Charnock

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血管内皮生长因子(VEGF)是一种强有力的分泌型血管生成生长因子。其作用是通过酪氨酸激酶受体Flt和KDR介导的。在这里,我们详细地研究了这种配体及其受体在整个妊娠过程中在人类胎盘中的分布。在妊娠早期,原位杂交显示Flt mRNA在绒毛滋养层周围的分布不均匀,显示出空间调节。妊娠中期胎盘绒毛组织中未检测到Flt基因的表达,足月绒毛组织中表达水平较低。在整个妊娠过程中,绒毛外滋养层细胞同时含有编码Flt和Flt样免疫反应的mRNA。相反,KDR mRNA仅与血管内皮细胞相关。在蜕膜内,抗Flt抗体在妊娠早期染色多种细胞类型,但在妊娠后期仅染色绒毛外滋养细胞。血管内皮生长因子免疫反应倾向于与Flt染色共同定位。这些结果表明,VEGF可能在胎盘绒毛和母体蜕膜中与滋养细胞的生长、分化和迁移有关,并且主要是通过对Flt受体而不是KDR受体的时空调节来实现的。
Vascular endothelial growth factor (VEGF) is a potent secreted angiogenic growth factor. Its action is mediated through the tyrosine kinase receptors flt and KDR. We here examine, in detail, the distribution of this ligand and its receptors in human placentae throughout gestation. In the first trimester, in-situ hybridization revealed uneven distribution of flt mRNA around the villous trophoblast indicating spatial regulation. Temporal regulation of flt was observed with no flt mRNA expression detected in villi from mid-gestational placenta, while low levels were found in term villi. Extravillous trophoblast was found to contain both mRNA encoding flt and flt-like immunoreactivity throughout pregnancy. In contrast, KDR mRNA was found only in association with endothelial cells. Within the decidua the anti-flt antibody stained multiple cell types during the first trimester of pregnancy but only the extravillous trophoblast later in gestation. VEGF immunoreactivity tended to co-localize with the staining for flt. These results indicate that VEGF may exert an important role within both the placental villi and the maternal decidua in relation to the growth, differentiation and migration of trophoblast and that this is mediated primarily through the spatial and temporal regulation of the flt receptor rather than the KDR receptor.