During development, cellular behavior is influenced by several factors. Amongst them, the extracellular matrix (MEC), a complex network of molecules, provides structural support and also functions as communicating ligands between cells. The MEC-cell interaction also depends on receptors on the cell surface, such as integrins, which are capable of triggering intracellular events associated with signal transduction cascades to promote cell differentiation, proliferation, death, and migration. During the embryo implantation, the trophoblast cells that line it interacts with the uterine ECM components to lodge the blastocyst in this tissue adequately. One of the components of the uterine ECM present during this process is the laminin, identified as an important inducer of cell proliferation and migration through activation of the MAPK pathway (mitogen-activated protein kinases, originally called ERK: kinases regulated by extracellular signal). However, if this signaling occurs in trophoblast cells, it has not yet been elucidated. In this context, our study hypothesis is that the interaction between endometrial laminin and integrins on the surface of trophoblast cells activate the MAPK-ERK pathway associated with cell proliferation and invasion processes in these cells. We will investigate this possibility through immunohistochemical analyzes, Western blotting assays, and specific pharmacological inhibitors of the MAPK-ERK pathway, using ectoplacental cones isolated from mouse blastocysts (7.5 days of gestation) embedded in a 3D support matrix system containing laminin.
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