Agnès Noël

TL;DR: It is reported that embryonic angiogenesis in mice was not affected by deficiency of PlGF, andTransplantation of wild-type bone marrow rescued the impairedAngiogenesis and collateral growth in Pgf−/− mice, indicating that PlGF might have contributed to vessel growth in the adult by mobilizing bone-marrow–derived cells.

TL;DR: It is reported here that deficient PAI1 expression in host mice prevented local invasion and tumor vascularization of transplanted malignant keratinocytes and this experimental evidence demonstrates that host-produced PAI is essential for cancer cell invasion and angiogenesis.

TL;DR: Two different pathophysiological mechanisms associated with preeclampsia are suggested, related to an overproduction of competitive soluble VEGFR-1 that may lead to suppression of VEGF-A and PlGF effects and the down-regulation of its membrane bound form in the placental bed, which may result in the defective uteroplacental development.

TL;DR: In vivo, ex vivo, and in vitro bioassays that are available for the evaluation of angiogenesis are described and critical aspects that are relevant for their execution and proper interpretation are highlighted.

TL;DR: It is demonstrated that miR-146a is a downstream-mediator of 16K PRL that could potentially serve as a biomarker and therapeutic target for PPCM.