Mouse early development involves a number of events requiring regulated extracellular proteolysis. Remarkably controlled tissue remodeling, cell migration and proliferation take place during hemochorial placenta formation in mouse and humans. To address the question of the role of uPA in the formation of the placental architecture in the mouse, we have studied placentation in uPA -/ and wild type mice. 13.5 day placentas were hybridized with probes for uPA, uPAR, PAI-1 and O2MR/LRP and specific markers for spongiotrophoblasts, giant cells and endothelial cells, and stained immunohistochemically for uPA, uPAR and PAI-1 antigens. First, we show that the components of the uPA system during placentation are precisely regulated. The main site of uPA synthesis in 13.5 day placenta appears to be the junctional zone, composed mainly of spongiotrophoblasts, derived from ectoplacental cone trophoblast cells. While the lack of uPA is not sufficient to prevent the formation of a functional placenta, uPA -/- junctional zone differs from that of wild type, being rather than a regular well defined layer, a disorganized structure, with strands of spongiotrophoblasts lagging behind in the adjacent labyrinthine layer. We are investigating whether this phenotype could be related to reduced or delayed migration of trophoblast cells in uPA -/- placentas. The lack of uPA could have more severe effects in different genetic backgrounds or in the absence of other proteolytic enzymes. Therefore, we are transferring the uPA null mutation into different mouse strains and mutants.
|Number of pages||1|
|Issue number||SUPPL. 3|
|Publication status||Published - 1996|
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