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Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis

ABSTRACT: Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis

PROVIDER: PRJNA549450 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR9320100.fastq.gz	Fastqsanger.gz
	SRR9320170.fastq.gz	Fastqsanger.gz
	SRR9320101.fastq.gz	Fastqsanger.gz
	SRR9320161.fastq.gz	Fastqsanger.gz

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

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

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

Project description: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 RNAseq)

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

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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.

2020-06-30 | GSE132914 | GEO

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 (mouse scRNAseq)

2020-06-30 | GSE132910 | GEO

Disease modeling of pulmonary fibrosis using human iPS cell-derived alveolar organoids (fibroblasts)

Project description:We developed an in vitro model of pulmonary fibrosis using alveolar organoids, consisting of human induced pluripotent stem cell-derived alveolar epithelial cells and human lung fibroblasts. In this model, fibroblasts were activated by bleomysin (BLM) treatment in an epithelial cell-dependent manner simillar to the pathogenic mechanism of pulmonary fibrosis.

2021-11-19 | GSE172121 | GEO

Disease modeling of pulmonary fibrosis using human iPS cell-derived alveolar organoids (SPC+ cells)

2021-11-19 | GSE172122 | GEO

Resetting proteostasis in aged animals with ISRIB prevents recruitment of profibrotic monocyte-derived alveolar macrophages during pulmonary fibrosis

Project description:Aging is among the most important risk factors for the development of pulmonary fibrosis. Inappropriate or prolonged activation of the integrated stress response has been implicated in the pathobiology of both aging and pulmonary fibrosis. We found that a small molecule that relieves translational inhibition induced by activation of the integrated stress response (ISRIB) attenuated the severity pulmonary fibrosis in young and old mice. We demonstrate that severe fibrosis in old mice was associated with increased number of pathogenic monocyte-derived alveolar macrophages. Using transcriptomic profiling we found that ISRIB modulates stress response signaling in alveolar epithelial cells resulting in decreased recruitment of pathogenic monocyte-derived alveolar macrophages. Thus our data suggest that inhibition of the integrated stress response in the lung epithelium can ameliorate pulmonary fibrosis by preventing the recruitment of monocyte-derived alveolar macrophages.

2021-04-16 | GSE145295 | GEO

Hyaluronan and TLR4 Regulate Alveolar Stem Cell Renewal and Prevent Severe Pulmonary Fibrosis

Project description:The successful repair of alveolar epithelial injury is required to restore the integrity of gas exchanging regions of the lung and preserve organ function. Severe pulmonary fibrosis is the result of repeated episodes of epithelial injury, activation of fibroblasts, and matrix accumulation. Thus, impaired alveolar epithelial progenitor cell renewal could contribute to the progression of fibrosis. We provide evidence that expression of TLR4 and hyaluronan (HA) on Type 2 alveolar epithelial cells (AEC2s) is necessary for self-renewal. Either deletion of TLR4 or HA synthase 2 leads to impaired regeneration of AEC2s, severe fibrosis and mortality, in part due to blunted production of IL-6. AEC2s from patients with pulmonary fibrosis have reduced cell surface HA, and impaired renewal capacity, suggesting that interactions between HA and TLR4 are key regulators of lung stem cell renewal, repair of lung injury and that severe pulmonary fibrosis is the result of epithelial stem cell failure. We used microarrays to detail the gene expression of AEC2 cells from WT and TLR4-/- mice.

2016-10-03 | GSE68704 | GEO

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