About Placental Growth Factor:
Placental growth factor (PlGF) is a member of the VEGF (vascular endothelial growth factor) sub-family which is a key molecule in angiogenesis and vasculogenesis, notably during embryogenesis. The primary source of PlGF during pregnancy is the placental trophoblast. PlGF can also be expressed in many other tissues such as the villous trophoblast.
Placental growth factor is ultimately associated with angiogenesis. PlGF plays a role in trophoblast growth and differentiation. Trophoblast cells such as extravillous trophoblast cells, are responsible for invading maternal arteries. Proper development of blood vessels in the placenta is crucial for proper embryonic development. Under normal physiologic conditions, PlGF is also expressed at a lower level in other organs like the heart, thyroid, lung and skeletal muscle.
Clinical Significance of Placental Growth Factor
PlGF expression in human atherosclerotic lesions is associated with plaque inflammation and neovascular growth. Serum levels of PlGF and SFLT-1 (soluble fms-like tyrosine-kinase-1 or VEGF receptor-1) are changed in women with pre-eclampsia, a disorder of pregnancy that is often characterized by the onset of high blood pressure and a significant amount of protein in the urine. Studies have shown that in both late and early onset pre-eclampsia, maternal serum levels of SFLT-1 are higher and PlGF lower in women presenting with pre-eclampsia.
Furthermore, placental SFLT-1 levels are significantly increased and PlGF decreased in women with preeclampsia compared to those with uncomplicated pregnancies. This seems to suggest that placental concentrations of SFLT-1 and PlGF mirror the maternal serum changes. These actions are consistent with the view that the placenta is the main source of SFLT-1 and PlGF during pregnancy.
PlGF in Reproduction
The pole of PlGF in reproduction is still being studied. PlGF is thought to be redundant in reproduction due to PlGF knockout mice being fertile. However, endometrial tissue during the secretory phase of the human menstrual cycle has shown to secrete PlGF. The presence of PlGF supports a role of PlGF in influencing embryo implantation, but this requires further characterization. PlGF knockout mice appear normal, but some differences in foetal and adult brain development have been discovered.
During the first trimester, concentrations of PlGF in women undergoing a normal pregnancy are low. This increases from week 11 to 12 onwards to a peak at the 30th week, where it decreases. This is in contrast with sFLT-1 which increases towards the conclusion of the pregnancy. This normal divergence of angiogenic factors levels occurs as the bioavailability of PlGF is reduced when it binds to SFLT-1. Regular levels of PlGF concentration are dependent on the gestational age.