ΔNp63 drives dysplastic alveolar remodeling and restricts epithelial plasticity upon severe lung injury.

ABSTRACT: The lung exhibits a robust, multifaceted regenerative response to severe injuries such as influenza infection, during which quiescent lung-resident epithelial progenitors participate in two distinct reparative pathways: functionally beneficial regeneration via alveolar type 2 (AT2) cell proliferation and differentiation, and dysplastic tissue remodeling via intrapulmonary airway-resident basal p63⁺ progenitors. Here we show that the basal cell transcription factor ΔNp63 is required for intrapulmonary basal progenitors to participate in dysplastic alveolar remodeling following injury. We find that ΔNp63 restricts the plasticity of intrapulmonary basal progenitors by maintaining either active or repressive histone modifications at key differentiation gene loci. Following loss of Δ

SUBMITTER: Weiner AI 

PROVIDER: S-EPMC9808897 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature