Expression of mRNA for vascular endothelial growth factor in human placenta
Implantation and growth of the placenta requires extensive angiogenesis to establish the vascular structures involved in exchange. Failure to establish adequate blood supply to the fetus may have serious clinical consequences such as intrauterine growth retardation. Vascular endothelial cell growth...
Saved in:
Published in: | Journal of reproduction & fertility Vol. 99; no. 2; pp. 609 - 615 |
---|---|
Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
Society for Reproduction and Fertility
01-11-1993
|
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Implantation and growth of the placenta requires extensive angiogenesis to establish the vascular structures involved in exchange.
Failure to establish adequate blood supply to the fetus may have serious clinical consequences such as intrauterine growth
retardation. Vascular endothelial cell growth factor (VEGF) is a recently identified growth factor with significant angiogenic
properties. We have demonstrated the presence of four species of mRNA encoding VEGF in both first trimester and term placenta.
In situ hybridization was used to localize the sites of expression of VEGF mRNA in these tissues. VEGF expression was seen in villous
trophoblast in the first trimester and in extravillous trophoblast at term, and in both fetal macrophages within the villi
and maternal macrophages in the decidua. Glandular epithelium in maternal decidua also expressed VEGF mRNA. The strongest
site of expression was in maternal macrophages adjacent to Nitabuch's stria, a zone of necrosis at the site of implantation.
This complex pattern of expression suggests that VEGF is involved in angiogenesis on both maternal and fetal sides of the
placenta and that macrophages are the primary source of VEGF. However, VEGF may also play a role in term placenta, when extensive
angiogenesis has diminished, possibly regulating vascular permeability. |
---|---|
ISSN: | 1470-1626 0022-4251 1741-7899 |
DOI: | 10.1530/jrf.0.0990609 |