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Abstract

The rapidly growing chorionic villi of the human placenta characteristically show constant blood vessel growth and differentiation. In contrast, the underlying decidua reveals tissue remodeling without apparent angiogenesis. Using the chick chorioallantoic membrane (CAM) assay, we found marked inhibition of angiogenesis by the feto-maternal interface tissue derived from nine human placentas obtained minutes after delivery. Inhibition was prevented by the addition of monensin, which blocks the release of synthesized cell products, and was markedly reduced by drying or freezing the tissue before the assay. Histology, combined with statistical analysis of the constituent cell types, correlated inhibition of angiogenesis with the number of fetally-derived extravillous trophoblasts in the feto-maternal interface tissue. Electron microscopy revealed endothelial cell damage in preexisting small (but not large) CAM vessels. We conclude that decidual tissue inhibited angiogenesis by releasing a water soluble factor which was under apparent constant production by vaible trophoblast on the CAM. The extravillous trophoblast population resembles tumor cells in its migratory and invasive properties but, in contrast to tumor induced angiogenesis, it is angiostatic, perhaps to counteract angiogenic proteins leaking from the intervillous space which could be detrimental to the maternal organism if active.

SEMA3B but Not CUL1 as Marker for Pre-Eclampsia Progression

“…The elevation of sFlt-1 was suggested to be an anti-angiogenic event leading to endothelium dysfunction and clinical PE syndrome. Increased sFlt-1 expression in the placenta of PE patients accompanied by an increase in maternal circulating sFlt-1 (or vice versa) may suggest clinical onset of the disease and even be associated with its severity (19, 20). The role of SEMA3B as anti-angiogenic factor is similar to that of sFlt-1 via downregulation of VEGF (12).…”