Author: Ali Gibran; Runzhen Zhao; Mo Zhang; Krishan G. Jain; Jianjun Chang; Satoshi Komatsu; Xiaohui Fang; Beiyun Zhou; Jiurong Liang; Dianhua Jiang; Mistuo Ikebe; Michael A Matthay; Hong-Long Ji
Title: Fibrinolytic niche is requested for alveolar type 2 cell-mediated alveologenesis and injury repair Document date: 2020_3_25
ID: 4h930ksd_17
Snippet: The primary objective of this study was to decipher the role of the fibrinolytic niche in the re-alveolarization mediated by progenitor AT2 cells and underlying mechanisms in healthy and injured lungs. We employed influenza-infected mice, Plau -/and Serpine1 Tg mouse strains, primary human AT2 cells from the human lungs of brain-dead patients with ARDS, and 3D organoids and polarized monolayers of AT2 cells to trace the cell fate in vivo and in v.....
Document: The primary objective of this study was to decipher the role of the fibrinolytic niche in the re-alveolarization mediated by progenitor AT2 cells and underlying mechanisms in healthy and injured lungs. We employed influenza-infected mice, Plau -/and Serpine1 Tg mouse strains, primary human AT2 cells from the human lungs of brain-dead patients with ARDS, and 3D organoids and polarized monolayers of AT2 cells to trace the cell fate in vivo and in vitro. The results demonstrate that the impaired fibrinolytic niche in influenza-infected lungs and genetically engineered mice modeling impaired fibrinolytic niche results in a significant decline in the proliferative AT2 and differentiated AT1 cells.
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