Differential Expression of Placenta Growth Factors and Their Receptors In the Normal and Pregnancy-Induced Hypertensive Human Placentas

Abstract

Placental development requires extensive angiogenesis and the invasion of the maternal decidua by the trophoblasts. Adequate and organized interaction of vascular endothelial growth factors (VEGF), placenta growth factors (PlGF), and their receptors are essential for a normal development and function of the placenta. In this study, we evaluated the expressions of PlGFs and their receptors, mRNAs by Northern blotting, in situ hybridization and RT-PCR in the normal and pregnancy-induced hypertensive (PIH) placentas. The expression level of PlGF-2 mRNA was lower in the PIH placentas compared to control as assessed by Northern blotting and in situ hybridization. PlGF mRNA was mainly localized to the vasculosyncytial membrane of placental villi and villous stroma. The expression of PlGF receptor-1 (PlGFR-1) was significantly increased in the PIH placentas compared to the normal ones. These results suggest that the alteration of PlGF-2 and PlGFR-1 mRNA expressions in the placenta are related to the pathogenesis of PIH.

Expression of placenta growth factor, soluble fms‐like tyrosine kinase‐1, metal‐responsive transcription factor‐1, heme oxygenase 1 and hypoxia inducible factor‐1α mRNAs in pre‐eclampsia placenta and the effect of pre‐eclampsia sera on their expression of choriocarcinoma cells

“…The PlGF levels in the peripheral blood of pre‐eclamptic women are lower than those in normal pregnant women . A decrease in PlGF mRNA expression has been reported in pre‐eclampsia placenta . This study confirmed that PlGF mRNA expression in pre‐eclampsia placenta was lower than that in normal pregnancy placenta.…”

Vascular Endothelial Growth Factor/Placental Growth Factor Heterodimer Levels in Preterm Infants with Bronchopulmonary Dysplasia

“…This heterodimer has weaker mitogenic activity, and its formation leads to depletion of VEGF homodimer levels and, consequently, of its angiogenic activity. [25][26][27] In addition, VEGF/PlGF induces the formation of sFlt-1. [28][29][30] Through these mechanisms, the VEGF/PlGF heterodimer contributes to the antiangiogenic state and consequent decrease in VEGF found in BPD.…”

Confocal laser scanning microscope study of cytokeratin immunofluorescence differences between villous and extravillous trophoblast: Cytokeratin downregulation in pre‐eclampsia

“…However, Smith et al (1999) concluded that reactive oxygen and nitrogen are not induced by TNF␣ and IFN␥ and do not mediate cytokine-induced apoptosis in this setting. Vascular endothelial growth factor (VEGF)-A and placental growth factor (PlGF) and their receptors are generally accepted to be required for healthy placental development, and alteration of PlGF-2 (lower) and PlGFR-1 (raised) mRNA expressions in the placenta are related to the pathogenesis of pregnancy-induced hypertension (Cho et al, 2003). Tsatsaris et al (2003) suggest two mechanisms of pre-eclamptic disease: 1) Overproduction of competitive soluble VEGFR-1 that leads to suppression of (VEGF)-A and PlGF mediated effects; and 2) Lowered membrane-bound (VEGFR-1) in the placental bed that results in defective uteroplacental development.…”