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Investigating the role of aging and lung fibrosis in Endothelial Cells with ATAC sequencing

ABSTRACT: In order to elucidate the contribute of the pulmonary vasculature to lung fibrosis, we injured young and aged mice with bleomycine, to create a model of resolving versus persistent lung fibrosis. The animals were sacrificed 30 days after the injury (time point in which we observed a divergent resolving vs persistent lung fibrosis in young vs aged mice).

ORGANISM(S): Mus musculus

PROVIDER: GSE177055 | GEO | 2022/05/09

REPOSITORIES: GEO

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Investigating the role of aging and lung fibrosis in Endothelial Cells with RNA sequencing

Project description:In order to elucidate the contribute of the pulmonary vasculature to lung fibrosis, we injured young and aged mice with bleomycine, to create a model of resolving versus persistent lung fibrosis. The animals were sacrificed 30 days after the injury (time point in which we observed a divergent resolving vs persistent lung fibrosis in young vs aged mice). We found that lung fibrosis resolution in young mice was accompained by the activation of transcriptional programs promoting vascular repair and lung fibrosis resolution. Lung endothelial cells from aged mice after injury failed to activate these programs, leading to dysrepair and progressive fibrosis.

2021-09-30 | GSE181508 | GEO

High-dimensional comparison of monocytes and T cells in post-COVID and idiopathic pulmonary fibrosis

Project description:Up to 30% of hospitalized COVID-19 patients experience persistent sequelae, including pulmonary fibrosis (PF). We examined COVID-19 survivors with impaired lung function and imaging worrisome for developing PF and found within six months, symptoms, restriction and PF improved in some (Early-Resolving COVID-PF), but persisted in others (Late-Resolving COVID-PF). To evaluate immune mechanisms associated with recovery versus persistent PF, we performed single-cell RNA-sequencing and multiplex immunostaining on peripheral blood mononuclear cells from patients with Early- and Late-Resolving COVID-PF and compared them to age-matched controls without respiratory disease. Our analysis showed circulating monocytes were significantly reduced in Late-Resolving COVID-PF patients compared to Early-Resolving COVID-PF and non-diseased controls. Monocyte abundance correlated with pulmonary function forced vital capacity and diffusion capacity. Differential expression analysis revealed MHC-II class molecules were upregulated on the CD8 T cells of Late-Resolving COVID-PF patients but downregulated in monocytes. To determine whether these immune signatures resembled other interstitial lung diseases, we analyzed samples from Idiopathic Pulmonary Fibrosis (IPF) patients. IPF patients had a similar marked decrease in monocyte HLA-DR protein expression compared to Late-Resolving COVID-PF patients. Our findings indicate decreased circulating monocytes is associates with decreased lung function and uniquely distinguishes Late-Resolving COVID-PF from Early-Resolving COVID-PF, IPF, and non-diseased controls.

2023-12-07 | GSE249513 | GEO

Comparative transcriptional analysis of lung fibroblasts from young and aged mice identifies PIM1/NFATc1 axis as a driver of persistent fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is an aging-associated disease characterized by the accumulation of myofibroblasts leading to the progressive scarring of the lung. To identify transcriptional gene programs driving persistent fibrosis in aged lungs, we performed a comparative RNA-seq analysis of fibroblasts freshly isolated from young and aged mouse lungs 30 days post-bleomycin injury. We discovered that lung fibroblasts isolated from young animals at this time point post-injury were transcriptionally similar to those isolated from uninjured mice. In contrast, aged lung fibroblasts isolated at the same time point exhibited a sustained pro-fibrotic state characterized by the elevated expression of genes implicated in inflammation, extracellular matrix remodeling, and cell survival. We identified the protein kinase pro-viral integration site of Moloney murine leukemia virus 1 (PIM1) and its direct target Nuclear Factor of Activated T Cells-1 (NFATc1) as putative drivers of the sustained profibrotic gene signatures observed in aged lung fibroblasts post-injury. PIM1 and NFATc1 transcripts were highly enriched in a pathogenic fibroblast population recently discovered in IPF lungs, and their protein expression was detected in fibroblastic foci. Overexpression of PIM1 in normal human lung fibroblasts potentiated their fibrogenic activation and this effect was dependent on NFATc1. Pharmacological inhibition of PIM1 in IPF-derived lung fibroblasts attenuated their activation and sensitized them to apoptotic stimuli. Finally, inhibition of PIM1 strongly reduced the expression of ECM remodeling and pro-survival genes and blocked the secretion of collagen in IPF lung explants ex vivo. Targeting PIM1/NFATc1 axis in pathogenic lung fibroblasts may represent a therapeutic strategy to limit their activation and promote fibrosis resolution in IPF.

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Project description:The intent of the experiment is to study the reactivity of human primary blood monocytes during a physiological or pathological inflammation. We designed two in vitro models that recapitulate the different phases of the reaction (recruitment, initiation, development, and resolution - \\"resolving model\\" - vs. persistence of inflammation \"persistent model): monocytes were exposed to different stimuli (microbial molecules, cytokines, and Immune complexes), and to sequential changes in microenvironmental conditions (temperature, hypoxia, amount of serum), at different time points (0, 4, 14, 24, 48 h for the resolving model and 0, 2, 4, 14, 24, 72, 96 h for the persistent model).

2020-06-30 | E-MTAB-8226 | biostudies-arrayexpress

Comparative transcriptional analysis of lung fibroblasts from young and aged mice identifies PIM1/NFATc1 axis as a driver of persistent fibrosis

Project description:Comparative transcriptional analysis of lung fibroblasts from young and aged mice identifies PIM1/NFATc1 axis as a driver of persistent fibrosis

| PRJNA790454 | ENA

Differential proteomics of the synaptosomal fraction from rat dentate gyrus identified the changes associated with aging-dependent cognitive decline

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2019-08-19 | PXD013172 | Pride

Investigating the role and mechanism of stress induced protein Sesn2 in aged-related adaptive response to cardiac ischemia reperfusion injury

Project description:Purpose: to reveal the myocardium transcriptomic profile shift pattern before/after Ischemia Reperfusion stress in young, aged, and Sesn2-knockout mice. The goals of this study are to compare the transcriptomic shift pattern among young, aged, and Sesn2-knockout to explore the caridoprotective mechanism of Sesn2 in Ischemia Reperfusion stress and the critical roles of Sesn2 in age-related adapting response to Ischemia Reperfusion stress. Methods: Myocardium transcriptome profiles of young (3-4 months) wild-type, aged (24-26 months) wild-type, and Sesn2-knockout (3-4 months) mice in normal physiological and Ischemia Reperfusion stressed conditions. Results: Sesn2 is critical to repress inflammation and maintain metabolic and mitochondria homeostasis in hearts under Ischemia Reperfusion stress, especially to aged hearts.

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scRNAseq of young vs. aged corneal epithelium

Project description:We performed single cell transcriptional profiling of mouse corneal epithelium in young vs. aged mice.

2022-12-19 | GSE182419 | GEO

Expression data from lung tissue of Zmpste24 defient or wildtype c57BL/6 mice

Project description:Idiopathic pulmonary fibrosis is a devastating aging-associated disease of unknown etiology. Despite that aging is a major risk factor, the mechanisms linking aging with this disease are uncertain, and experimental models to explore them in lung fibrosis are scanty. We examined the fibrotic response to bleomycin-induced lung injury in Zmpste24-deficient mice, which exhibit nuclear lamina defects developing accelerated aging. We found that young WT and Zmpste24(-/-) mice developed a similar fibrotic response to bleomycin. Unexpectedly, while old WT mice developed severe lung fibrosis, accelerated aged Zmpste24-/- mice were protected showing scant lung damage. To investigate possible mechanisms associated with this resistance to fibrosis, we compared the transcriptome signature of the lungs and found that Zmpste24(-/-) mice showed downregulation of several core and associated matrisome genes compared with WT mice. Interestingly, some microRNAs that target extracellular matrix molecules such as miR23a, miR27a, miR29a, miR29b-1,miR145a, and miR491 were dysregulated resulting in downregulation of profibrotic pathways such as TGF-β/SMAD3/NF-κB and Wnt3a/β-catenin signaling axis. These results indicate that the absence of Zmpste24 in aging mice results in impaired lung fibrotic response after injury, which is likely associated to the dysregulation of fibrosis-related miRNAs. Aging is a driving force of pulmonary fibrosis. Mice laking Zmpste24 have an accelerated aging phenotype. During the development of the disease there are several extracellular matrix genes, principally collagens upregulated. We use microarray to unveil changes associated with the pulmonary response in aged mice

2018-12-04 | GSE123293 | GEO

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