Determinants of placental vascularity
DS Torry, M Hinrichs, RJ Torry - American journal of …, 2004 - Wiley Online Library
DS Torry, M Hinrichs, RJ Torry
American journal of reproductive immunology, 2004•Wiley Online LibraryProblem: Vascular growth during implantation and placentation is critical for successful
gestation and it is thought that vascular insufficiencies during placentation contribute to a
number of obstetrical complications. However, relatively little is known regarding the
regulation of angiogenesis in the placenta. Method of study: We review literature concerning
the potential significance of inadequate placental vascularity as a contributor to the
obstetrical complications of spontaneous abortion, fetal growth restriction and preeclampsia …
gestation and it is thought that vascular insufficiencies during placentation contribute to a
number of obstetrical complications. However, relatively little is known regarding the
regulation of angiogenesis in the placenta. Method of study: We review literature concerning
the potential significance of inadequate placental vascularity as a contributor to the
obstetrical complications of spontaneous abortion, fetal growth restriction and preeclampsia …
Problem: Vascular growth during implantation and placentation is critical for successful gestation and it is thought that vascular insufficiencies during placentation contribute to a number of obstetrical complications. However, relatively little is known regarding the regulation of angiogenesis in the placenta.
Method of study: We review literature concerning the potential significance of inadequate placental vascularity as a contributor to the obstetrical complications of spontaneous abortion, fetal growth restriction and preeclampsia. Gene expression assays were used to compare fluctuations of placenta growth factor (PlGF) and PlGF receptor expression in normal and preeclamptic trophoblast in vitro.
Results: Studies have shown that common obstetrical complications manifest altered placental vascularity. Both intrinsic defects (gene knockouts) and extrinsic factors (O2 tension, cytokines, etc) may be responsible for the defects. Some of these factors have been shown to influence trophoblast vascular endothelial growth factor (VEGF)/PlGF expression suggesting this particular family of angiogenic proteins play an important role in placental angiogenesis.
Conclusion: Placental vascularization reflects a complex interaction of regulatory factors. Understanding the regulation of vascular growth in the placenta will provide much needed insight into placenta‐related vascular insufficiencies.
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