Cell adhesion and communication in the corpus luteum-Function and regulation of tight and adherens junctions in the luteal vascular systemTranslation into pathophysiology Regulation of permeability in ovarian cancer

从以往的研究可知，多种细胞角蛋白和生长因子参与粘附蛋白的调控和通透性的调控。我们已经在人黄体模型中证明了hCG介导的VEGF与粘附蛋白VE-cadherin， claudin 5和nectin 2之间的通透性的生理调节。除了hCG / VEGF /粘附蛋白相互作用外，我们还研究了第二个系统，Robo / Slit系统。在那里，我们能够在CL中发现直接依赖vegf的Slit 2/Robo下调。基于这些积极的发现，我们首次研究了卵巢癌腹水的通透性调节。在这里，我们能够检测到VEGF和claudin5之间的调节系统，从而增加了通透性。根据这些数据，我们现在想集中研究更多关于黄体中粘附蛋白VE-cadherin， claudin 5和nectin 2的细节，以及它们在CL和人卵巢癌的生理和病理生理模型中与Robo / Slit系统的相互作用。

From previous studies it is known that various cytokeratins and growth factors are involved in the regulation of adhesion proteins and in the regulation of permeability.We already demonstrated a physiological hCG mediated regulation of permeability between VEGF and the adhesion proteins VE-cadherin, claudin 5 and nectin 2 in an human corpus luteum model. Regardless of the hCG / VEGF / adhesion protein interaction we also examined a second system, the Robo / Slit system. There, we were able to find a direct VEGF-dependent downregulation of Slit 2/Robo in the CL. Based on these positive findings we firstly examined the permeability regulation of the human ovarian cancer ascites. Here we were able to detect a regulatory system between VEGF and claudin 5 with consequently increased permeability.With recourse to this pdata, we would now like to focus on the examination of more details about the adhesion proteins VE-cadherin, claudin 5 and nectin 2 in the corpus luteum as well as their interaction with the Robo / Slit System in physiological and pathophysiological models of the CL and the human ovarian cancer.