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Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis (mouse_bulk RNAseq)

ABSTRACT: bulk RNAseq comparison of global transcription profiles of mouse lung AT2 Sin3a-LOF at different time points, evalute AT2 cellular senescecne contribution to lung fibrosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE132909 | GEO | 2020/06/30

REPOSITORIES: GEO

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Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis (human)

Project description:Idiopathic pulmonary fibrosis (IPF) is a fatal form of interstitial lung disease associated with progressive scarring of lung tissue and declining pulmonary function in aging individuals. Here we employ data mining and single cell RNA sequencing (scRNAseq) to define candidate drivers of AT2 senescence in IPF lung tissue. We show that AT2 cells isolated from IPF lung tissue exhibit characteristic features of cellular senescence and reduced abundance of Sin3a, critical determinant of endodermal progenitor cell maintenance in the developing lung. Conditional loss of Sin3a within AT2 cells of the adult mouse lung activated a program of p53-dependent cellular senescence and AT2 cell depletion, leading to progressive pulmonary fibrosis. In contrast, ablation of AT2 cells through conditional activation of a DTA toxin gene led to transient fibrosis that resolved over time, suggesting that senescence of AT2 cells was a critical driver of progressive fibrosis. Activation of b6 integrin was observed within a subset of AT2 cells with Sin3a loss-of-function that localized to the advancing margin of advancing fibroproliferative lesions. Systemic inhibition of TGF signaling or delivery of senolytic drugs prevented lung fibrosis in Sin3a loss-of-function mice. Our findings establish a novel mouse model that recapitulates key pathological features of human IPA and show that p53-dependent senescence is a proximal regulator of TGF induction and progressive pulmonary fibrosis.

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Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis (mouse scRNAseq)

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Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis (mouse bulk AT2)

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Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis (mouse bulk AT2)

Project description:Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis (mouse bulk AT2)

| PRJNA549446 | ENA

Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-30 | GSE132915 | GEO

Integrated multiomic analysis identifies TRIP13 as a mediator of alveolar epithelial type II cell dysfunction in idiopathic pulmonary fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is a lethal progressive lung disease urgently needing new therapies. Current treatments only delay disease progression, leaving lung transplant as the sole remaining option. Recent studies support a model whereby IPF arises because alveolar epithelial type II (AT2) cells, which normally mediate distal lung regeneration, acquire airway and/or mesenchymal characteristics, preventing proper repair. Mechanisms driving this abnormal differentiation remain unclear. We performed integrated transcriptomic and epigenomic analysis of purified AT2 cells which revealed genome-wide alterations in IPF lungs. The most prominent epigenetic alteration was activation of an enhancer in thyroid receptor interactor 13 (TRIP13), coinciding with TRIP13 upregulation. TRIP13 is broadly implicated in epithelial-mesenchymal plasticity and transforming growth factor-beta signaling. In cultured human AT2 cells and lung slices, small molecule TRIP inhibitor DCZ0415 prevented acquisition of the mesenchymal gene signature characteristic of IPF, suggesting TRIP13 inhibition as a potential therapeutic approach to fibrotic disease.

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