Activation Of Airway Resident Sox2 Lin гђ Progenitor Cells In Response

Activation Of Airway Resident Sox2 Lin гђ Progenitor Cells Activation of airway resident sox2 lin − progenitor cells in response to influenza induced severe lung injury the schematic shows that following pr8 influenza virus infection induced lung injury sox2 lin − progenitor cells are the major source of nascent krt5 cells in the airway and alveolar zones of cell loss. Download scientific diagram | activation of airway resident sox2 lin À progenitor cells in response to influenza induced severe lung injury the schematic shows that following pr8 influenza.

Activation Of Airway Resident Sox2 Lin гђ Progenitor Cells Stripp and colleagues report that h1n1 influenza virus infection in mice induces distal lung epithelial remodeling marked by the appearance of nascent krt5 cells in injured airways and alveoli. rather than pre existing basal, club, and alveolar progenitor cells, they traced the cellular origin of these nascent krt5 cells to a population of airway resident sox2 lin− progenitor cells. Sox2 is required for normal airway epithelial cell proliferation and the differentiation of distinct subsets of cells lining bronchioles, including ciliated, goblet, and nonciliated secretory cells. sox2 is dynamically regulated after injury of the airways, activating cell proliferation and enhancing differentiation of airway progenitor cells. These data suggest that airway cell identity is maintained at homeostasis by sox2 and upon its loss, secretory cells acquire a more basc at2 signature while basal like progenitor cells increase. Figure 4. activation of airway resident sox2 lin progenitor cells in response to influenza induced severe lung injury "rare sox2 airway progenitor cells generate krt5 cells that repopulate damaged alveolar parenchyma following influenza virus infection".

Activation Of Airway Resident Sox2 Lin гђ Progenitor Cells These data suggest that airway cell identity is maintained at homeostasis by sox2 and upon its loss, secretory cells acquire a more basc at2 signature while basal like progenitor cells increase. Figure 4. activation of airway resident sox2 lin progenitor cells in response to influenza induced severe lung injury "rare sox2 airway progenitor cells generate krt5 cells that repopulate damaged alveolar parenchyma following influenza virus infection". The contribution of resident airway basal cells to the gener ation of krt5 alveolar pods have provided varied results, which, at least in part, could be attributed to differences. We sought to determine the cellular dynamics of lung repair following influenza infection and define whether nascent krt5 cells repopulating alveolar epithelium were derived from pre existing alveolar or airway progenitor cells. we found that the wound healing response begins with proliferation of sox2 scgb1a1 krt5 progenitor cells in airways.