![]() Ribera, Jordi Pauta, Montse Melgar-Lesmes, Pedro Córdoba, Bernat Bosch, Anna Calvo, Maria Rodrigo-Torres, Daniel Sancho-Bru, Pau Mira, Aurea Jiménez, Wladimiro Morales-Ruiz, Manuel All rights reserved.Ī small population of liver endothelial cells undergoes endothelial-to-mesenchymal transition in response to chronic liver injury. In conclusion, the transition from mesenchymal towards amoeboid movement highlights a molecular plasticity mechanism in endothelial cell migration in skin fibrosis. Interestingly, the migration of HMEC-1 undergoing EndMT is dependent on both ECM degradation and invadosome formation associated with MMP-2 proteolytic activity and Rho/ROCK cytoskeleton contraction. In parallel, MMP-2 is upregulated and is responsible for most proteolytic activity. We observed that TGF-Î☢ induces up to an intermediate mesenchymal phenotype in HMEC-1. We characterized the response of HMEC-1 to TGF-Î☢, a well-known mediator of EndMT within the microvasculature. ![]() Here, we hypothesized that microvascular endothelial cells (HMEC-1) undergoing EndMT adopt an intermediate state of drifting migration model between the mesenchymal and amoeboid protrusive types in the early stages of fibrosis. It may be either a Rho/ROCK-independent, an integrin- and MMP-correlated ECM degradation-dependent, a mesenchymal model or Rho/ROCK-dependent, integrin adhesion- and MMP activity-independent, an amoeboid model. The migration model of fibroblasts and fibroblast-resembling cells is still not fully understood. The contribution of endothelial cells to scar and fibrotic tissue formation is undisputedly connected to their ability to undergo the endothelial-to-mesenchymal transition ( EndMT) towards fibroblast phenotype-resembling cells. Kryczka, Jakub Przygodzka, Patrycja Bogusz, Helena Boncela, Joanna HMEC-1 adopt the mixed amoeboid- mesenchymal migration type during EndMT. This review will focus on summarizing the currently understood signaling pathways and epigenetic modifications involved in the regulation of EndMT and the role of EndMT in pathophysiological conditions of the cardiovascular system. ![]() Thus, comprehensive understanding of the underlying mechanisms of EndMT will provide novel therapeutic strategies to overcome congenital heart disease due to abnormal development and other cardiovascular diseases. EndMT contributes to steps in cardiovascular development, such as cardiac valve formation and septation, as well as the pathogenesis of various cardiovascular disorders, such as congenital heart disease, myocardial fibrosis, myocardial infarction and pulmonary arterial hypertension. Recent studies have identified the essential role of EndMT in the cardiovascular system. It has been demonstrated that epigenetic modifications are also involved in this process. A variety of stimuli, such as inflammation, growth factors, and hypoxia, regulate EndMT through various signaling pathways and intracellular transcription factors. It is a process that is characterized by the loss of features of endothelial cells and acquisition of specific markers of mesenchymal cells. ![]() Gong, Hui Lyu, Xing Wang, Qiong Hu, Min Zhang, XiangyuĮndothelial to mesenchymal transition ( EndMT) is a special type of epithelial to mesenchymal transition. Endothelial to mesenchymal transition in the cardiovascular system.
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