Abstract
Objective: The alveolar epithelium, consisting of mainly alveolar epithelial type 1 (AT1) and type 2 (AT2) cells, represents a major site of tissue destruction in idiopathic pulmonary fibrosis. Several studies indicate that adult AT2 cells are able to self-renew and exert progenitor function for AT1 cells upon alveolar injury in vivo. However, cell differentiation pathways enabling this plasticity are poorly understood. Here, we used the primary culture of murine AT2 cells as model system to identify novel proteins and pathways involved in epithelial transdifferentiation.
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