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Introduction The semi-permeable vascular barrier between the blood and the surrounding tissue is maintained by a monolayer of endothelial cells ( 1 ). The endothelial barrier regulates the extravasation of leukocytes and fluid ( 2 , 3
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Lung endothelial barrier dysfunction is the hallmark of Acute Respiratory Distress Syndrome (ARDS), the most severe form of Acute Lung Injury. In ARDS, pulmonary interstitial and alveolar edema augments the intra-pulmonary shunt and reduces the
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Leeuwenhoek Centre for Advanced Microscopy, Section Molecular Cytology at Swammerdam Institute for Life Sciences at University of Amsterdam, Amsterdam, the Netherlands
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local disruption of the endothelial barrier. Additionally, CTCs secrete factors that increase vascular permeability or induce apoptosis or necroptosis in ECs ( 5 , 7 , 8 , 9 ). CTCs can subsequently transmigrate through the barrier by forming membrane
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metabolites, proteins and leukocytes between the two compartments. Material can cross the endothelial barrier via both transcellular and paracellular routes ( 2 ). For transcellular transport, ECs deploy a diverse set of channels, transporters, pores and
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Department of Medical Specializations – Cardiology, University of Geneva, Geneva, Switzerland
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Department of Medical Specializations – Cardiology, University of Geneva, Geneva, Switzerland
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endothelial barrier function resulting in increased vascular permeability is a key event in pathological conditions associated with edema and inflammation. Although the endothelial barrier is principally regulated by tight junctions (TJs) sealing the
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.1056/NEJM198211183072103 ) 27 Mangialardi G Katare R Oikawa A Meloni M Reni C Emanueli C Madeddu P . Diabetes causes bone marrow endothelial barrier dysfunction by activation of the RhoA-Rho-associated kinase signaling pathway . Arteriosclerosis
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crawling on the luminal side of the endothelium allows the immune cells to find the endothelial junctions, which allow for their diapedesis across the endothelial barrier (reviewed in ( 3 )). Before reaching the tissue parenchyma, immune cells have to cross
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stabilizing Tie-2-Ang1 pathway, thus re-establishing endothelial barrier function ( 24 ). Alternatively or in addition to endothelial cell targeting, forced pericyte maturation by inhibiting PDGF-B signalling using a single-stranded nucleic acid
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vasorelaxation through altering EC responsiveness to nitric oxide and to reduction of endothelial barrier functions ( 14 ). IL1B can also act indirectly on ECs by stimulating the production of angiogenic factors. In the tumour microenvironment, expression of IL1B
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-020-09746-6 ) 37 Uwamori H Ono Y Yamashita T Arai K Sudo R . Comparison of organ-specific endothelial cells in terms of microvascular formation and endothelial barrier functions . Microvascular Research 2019 122 60 – 70 . ( https://doi.org/10.1016/j.mvr.2018
