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Fibrinolytic niche is requested for alveolar type 2 cell-mediated alveologenesis and injury repair
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covidontheweb.inria.fr
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Academic Article
research paper
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Covid-on-the-Web dataset
title
Fibrinolytic niche is requested for alveolar type 2 cell-mediated alveologenesis and injury repair
Creator
Ji, Hong-Long
Fang, Xiaohui
Matthay, Michael
Chang, Jianjun
Gibran, Ali
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source
BioRxiv
abstract
COVID-19, SARS, and MERS are featured by fibrinolytic dysfunction. To test the role of the fibrinolytic niche in the regeneration of alveolar epithelium, we compared the self-renewing capacity of alveolar epithelial type 2 (AT2) cells and its differentiation to AT1 cells between wild type (wt) and fibrinolytic niche deficient mice (Plau−/− and Serpine1Tg). A significant reduction in both proliferation and differentiation of deficient AT2 cells was observed in vivo and in 3D organoid cultures. This decrease was mainly restored by uPA derived A6 peptide, a binding fragment to CD44 receptors. The proliferative and differential rate of CD44+ AT2 cells was greater than that of CD44− controls. There was a reduction in transepithelial ion transport in deficient monolayers compared to wt cells. Moreover, we found a marked suppression in total AT2 cells and CD44+ subpopulation in lungs from brain dead patients with acute respiratory distress syndrome (ARDS) and a mouse model infected by influenza viruses. Thus, we demonstrate that the fibrinolytic niche can regulate AT2-mediated homeostasis and regeneration via a novel uPA-A6-CD44+-ENaC cascade.
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2020-03-25
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10.1101/2020.03.24.006270
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biorxiv
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de1f46387f76cec40f588d61832e3acbf2088707
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https://doi.org/10.1101/2020.03.24.006270
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Fibrinolytic niche is requested for alveolar type 2 cell-mediated alveologenesis and injury repair
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bioRxiv
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named entity 'reduction'
named entity 'AT2'
named entity 'CD44'
named entity 'infected'
named entity 'peptide'
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