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http://conacyt.repositorioinstitucional.mx/jspui/handle/1000/4243| Fibrinolytic niche is requested for alveolar type 2 cell-mediated alveologenesis and injury repair | |
| Gibran Ali. Zhao Runzhen. Zhang Mo. Jain Krishan. Chang Jianjun. Komatsu Satoshi. Fang Xiaohui. Zhou Beiyun. Liang Jiurong. Jiang Dianhua. Ikebe Mistuo. Matthay Michael. Ji Hong-Long. | |
| Acceso Abierto | |
| Atribución-NoComercial-SinDerivadas | |
| 10.1101/2020.03.24.006270 | |
| 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 Serpine1 Tg ). 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. | |
| www.biorxiv.org | |
| 2020 | |
| Artículo | |
| https://www.biorxiv.org/content/biorxiv/early/2020/03/25/2020.03.24.006270.full.pdf | |
| Inglés | |
| VIRUS RESPIRATORIOS | |
| Aparece en las colecciones: | Artículos científicos |
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