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However, relatively little is known regarding the regulation of angiogenesis in the placenta.<\/jats:p><jats:p><jats:bold>Method of study:\u2002<\/jats:bold> 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 <jats:italic>in vitro<\/jats:italic>.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> Studies have shown that common obstetrical complications manifest altered placental vascularity. Both intrinsic defects (gene knockouts) and extrinsic factors (O<jats:sub>2<\/jats:sub> 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.<\/jats:p><jats:p><jats:bold>Conclusion:\u2002<\/jats:bold> Placental vascularization reflects a complex interaction of regulatory factors. 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