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The aim of the present study was to quantify endothelial cell density in rat endometrium during early pregnancy (a time of increased endothelial cell proliferation), using immunohistochemical methods. Despite the occurrence of vessel growth, the endometrial endothelial cell density remained unchanged before embryo implantation, indicating that endothelial cell proliferation keeps pace with proliferation of the surrounding endometrial cells. After implantation, endothelial cell density falls at embryo sites on day 6, despite very high endothelial cell proliferation rates. This is probably due to the oedema caused by the localized increase in vascular permeability at implantation sites. We hypothesize that this reduction may provide a stimulus for the observed endothelial cell proliferation, rather than a direct angiogenic stimulus from the embryo.
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Peter A. W. Rogers (1995) studied this question.
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