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Aberrant Transitional Alveolar Epithelial Cells Promote Pathogenic Activation of Lung Fibroblasts in Preclinical Fibrosis Modeling (Bulk RNA-Seq)

ABSTRACT: Aberrant Transitional Alveolar Epithelial Cells Promote Pathogenic Activation of Lung Fibroblasts in Preclinical Fibrosis Modeling (Bulk RNA-Seq)

PROVIDER: PRJNA1140210 | ENA |

REPOSITORIES: ENA

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Aberrant Transitional Alveolar Epithelial Cells Promote Pathogenic Activation of Lung Fibroblasts in Preclinical Fibrosis Modeling (scRNAseq)

Project description:Aberrant Transitional Alveolar Epithelial Cells Promote Pathogenic Activation of Lung Fibroblasts in Preclinical Fibrosis Modeling (scRNAseq)

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Aberrant Transitional Alveolar Epithelial Cells Promote Pathogenic Activation of Lung Fibroblasts in Preclinical Fibrosis Modeling (Bulk RNA-Seq)

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Project description:Repeated injury of the lung epithelium is proposed to be the main driver of idiopathic pulmonary fibrosis (IPF). However, available therapies do not specifically target the epithelium and human models of fibrotic epithelial damage with suitability for drug discovery are lacking. We developed a model of the aberrant epithelial reprogramming observed in IPF using alveolar organoids derived from human-induced pluripotent stem cells stimulated with a cocktail of pro-fibrotic and inflammatory cytokines. Deconvolution of RNA-seq data of alveolar organoids indicated that the fibrosis cocktail rapidly increased the proportion of transitional cell types including the KRT5 - /KRT17 + aberrant basaloid phenotype recently identified in the lungs of IPF patients. We found that epithelial reprogramming and extracellular matrix (ECM) production persisted after removal of the fibrosis cocktail. We evaluated the effect of the two clinically approved compounds for IPF, nintedanib and pirfenidone, and found that they reduced the expression of ECM and pro-fibrotic mediators but did not completely reverse epithelial reprogramming. Thus, our system recapitulates key aspects of IPF and is a promising system for drug discovery.

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Regulation of the Alveolar Epithelial Transitional State in Murine and Human Pulmonary Fibrosis

Project description:Idiopathic Pulmonary Fibrosis (IPF) is a progressive scarring disease arising from impaired regeneration of the alveolar epithelium after injury. During regeneration, type 2 alveolar epithelial cells (AEC2s) differentiate into AEC1s via a transitional state that upregulates keratin 8. In IPF, transitional AECs persist with ineffectual AEC1 differentiation. However, whether keratin 8 regulates transitional state persistence and fibrosis is unclear. Here, we isolated AEC2s from WT or keratin 8 KO mice and harvested RNA from freshly isolated cells or from cells cultured for 1, 3, or 7 days. RNAseq was performed.

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Project description:Modeling of Aberrant Epithelial Reprogramming in Idiopathic Pulmonary Fibrosis using Human Induced Pluripotent Stem Cell-derived Alveolar Organoids

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