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CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE247272 | GEO | 2024/04/17

REPOSITORIES: GEO

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CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair.

Project description:Cell plasticity theoretically extends to all possible cell types, but naturally decreases as cells differentiate, whereas injury-repair re-engages the developmental plasticity. Here we show that the lung alveolar type 2 (AT2)-specific transcription factor (TF), CEBPA, restricts AT2 cell plasticity in the mouse lung. AT2 cells undergo transcriptional and epigenetic maturation postnatally. Without CEBPA, both neonatal and mature AT2 cells reduce the AT2 program, but only the former reactivate the SOX9 progenitor program. Sendai virus infection bestows mature AT2 cells with neonatal plasticity where Cebpa mutant, but not wild type, AT2 cells express SOX9, as well as more readily proliferate and form KRT8/CLDN4+ transitional cells. CEBPA promotes the AT2 program by recruiting the lung lineage TF NKX2-1. The temporal change in CEBPA-dependent plasticity reflects AT2 cell developmental history. The ontogeny of AT2 cell plasticity and its transcriptional and epigenetic mechanisms have implications in lung regeneration and cancer.

| S-EPMC10760240 | biostudies-literature

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [1]

2024-04-18 | GSE247130 | GEO

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [scATAC-seq]

2024-04-16 | GSE264098 | GEO

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [ChIP-seq]

2024-04-19 | GSE247271 | GEO

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair

Project description:CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair

| PRJNA1037034 | ENA

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [1]

Project description:CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [1]

| PRJNA1036384 | ENA

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [ChIP-seq]

Project description:CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [ChIP-seq]

| PRJNA1037037 | ENA

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [scATAC-seq]

Project description:CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [scATAC-seq]

| PRJNA1100986 | ENA

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

Project description: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 ΔNp63, intrapulmonary basal progenitors are capable of either airway or alveolar differentiation depending on their surrounding environment both in vitro and in vivo. Uncovering these regulatory mechanisms of dysplastic repair and lung basal cell fate choice highlight potential therapeutic targets to promote functional alveolar regeneration following severe lung injuries.

| S-EPMC9808897 | biostudies-literature

FGFR2b signalling restricts lineage-flexible alveolar progenitors during mouse lung development and converges in mature alveolar type 2 cells.

Project description:The specification, characterization, and fate of alveolar type 1 and type 2 (AT1 and AT2) progenitors during embryonic lung development are poorly defined. Current models of distal epithelial lineage formation fail to capture the heterogeneity and dynamic contribution of progenitor pools present during early development. Furthermore, few studies explore the pathways involved in alveolar progenitor specification and fate. In this paper, we build upon our previously published work on the regulation of airway epithelial progenitors by fibroblast growth factor receptor 2b (FGFR2b) signalling during early (E12.5) and mid (E14.5) pseudoglandular stage lung development. Our results suggest that a significant proportion of AT2 and AT1 progenitors are lineage-flexible during late pseudoglandular stage development, and that lineage commitment is regulated in part by FGFR2b signalling. We have characterized a set of direct FGFR2b targets at E16.5 which are likely involved in alveolar lineage formation. These signature genes converge on a subpopulation of AT2 cells later in development and are downregulated in AT2 cells transitioning to the AT1 lineage during repair after injury in adults. Our findings highlight the extensive heterogeneity of pneumocytes by elucidating the role of FGFR2b signalling in these cells during early airway epithelial lineage formation, as well as during repair after injury.

| S-EPMC9708820 | biostudies-literature

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