Placental growth factor (PlGF)
What is PlGF and why is it important?
Placental growth factor (PlGF) is a protein-coding gene that plays a key role in angiogenesis and vasculogenesis, in particular during embryogenesis. Angiogenesis is the development of new blood vessels and vasculogenesis is the process of blood vessel formation in the embryo. Proper development of blood vessels in the placenta is crucial for proper embryonic development.
PlGF and pre-eclampsia
Placental growth factor (PlGF) is a potential biomarker for pre-eclampsia, a condition in which blood vessels in the placenta are too narrow, resulting in high blood pressure.
Studies show that in both early and late onset pre-eclampsia, maternal serum levels of sFlt-1 (soluble fms-like tyrosine kinase-1) are higher and PlGF lower in women presenting with pre-eclampsia as compared to those with uncomplicated pregnancies.
Where is PlGF produced in the human body?
The main source of PlGF during pregnancy is the placental trophoblast. The placenta forms during pregnancy to support the growth and development of the foetus. Trophoblasts are specialized cells of the placenta that play an important role in embryo implantation and interaction with the maternal uterus.
Under normal physiologic conditions, PlGF is also expressed at a low level in other organs including the heart, lung, thyroid and skeletal muscle.
Pre-eclampsia, placental growth factor (PlGF) and pregnancy
Trophoblasts are cells forming the outer layer of a blastocyst that provides nutrients to the embryo, and develops into a large part of the placenta. They are formed during the first stage of pregnancy and are the first cells to differentiate from the fertilized egg. In terms of fetal-maternal communication, it is mainly the trophoblasts that coordinate the complex interactions between the fetus and mother.
Not only do placental trophoblasts provide structural and biochemical barriers between the mother and fetus during pregnancy, they also serve as an important endocrine organ that produces numerous growth factors and hormones that support and regulate placental and fetal development and growth. Furthermore, a successful pregnancy also largely depends on the angiogenic function of the trophoblast itself i.e., its ability to invade maternal myometrial spiral arteries (during the first trimester) and the capacity to generate growth factors that vascularize the placenta during its mid to later development (second and early third trimester).
Cytotrophoblast cells are the inner layer of the trophoblast. Fetal cytotrophoblasts invade the maternal uterine wall and move into the uterine spiral arteries. As a result of this invasion process, there is a loss of elasticity and an increase in the luminal diameter of the spiral arteries. Consequently, the spiral arteries are remodelled into large vessels with high capacity and low resistance. Pre-eclampsia is associated with shallow or inadequate cytotrophoblast invasion. The cytotrophoblast invasion of the uterus is only superficial, and the endovascular invasion does not proceed beyond the superficial layers of the spiral arterioles.
The process of trophoblast invasion is normally completed by 20 to 22 weeks of gestation in normal pregnancy. However, in cases of pre-eclampsia it has been found that cytotrophoblast invasion of the uterine spiral arterioles is often incomplete by this time and spiral arteries fail to lose their muscular elastic components resulting in vessels with decreased capacity and increased resistance. As a consequence of decreased blood flow, the fetus is not supplied with sufficient oxygen and nutrients.