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Gene expression profile at single cell level of p16INK4a+ fibroblasts from fibrotic mouse lung

ABSTRACT: Gene expression profile at single cell level of p16INK4a+ fibroblasts from fibrotic mouse lung

PROVIDER: PRJNA985733 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24975963.fastq.gz	Fastqsanger.gz
	SRR24975964.fastq.gz	Fastqsanger.gz

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Gene expression profile at single cell level of p16INK4a+ fibroblasts from fibrotic mouse lung

Project description:We studied the role of p16INK4a+ fibroblasts in lung fibrosis. We used single cell RNA seq (scRNA-seq) to characterize p16INK4a+ fibroblasts in fibrotic lung.

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Expression data from fibroblasts cultured from normal and fibrotic human lung tissue

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Acellular ECM Proteomics: Versican expression from lung fibroblasts is an autologous fibrotic brake

Project description:The activation and accumulation of lung fibroblasts, leading to excessive extracellular matrix (ECM) deposition, is a pathogenic hallmark of Idiopathic Pulmonary Fibrosis (IPF), a lethal and currently incurable disease. The collagen-rich fibrotic ECM perpetuates fibroblast activation and accumulation, which includes the promotion of podosome formation and ECM invasion. Proteoglycans (PGs), a significant component of the interstitial ECM, fine-tune the overall tissue architecture determined by fibrous proteins and regulate several ECM-controlled signalling pathways. In this report, increased expression of Versican (VCAN ), a multifunctional PG, was detected in human and mouse pulmonary fibrosis, predominantly in monocytic cells and fibroblasts. Genetic reduction of Vcan expression in mice promoted collagen expression and modulated pulmonary ECM composition and structure, exacerbating pulmonary fibrosis and delaying its resolution. Reduced ECM Vcan levels resulted in longer, thicker, and more tangled collagen fibrils, which stimulated podosome formation in fibroblasts and their ECM invasion. Moreover, the decrease of Vcan in the ECM and the ensuing reorganisation stimulated Tenascin-C (TNC) expression from fibroblasts, which was further shown to be a potent, TLR4-dependent, autologous podosome inducer, promoting ECM invasion. Thus, Vcan expression from fibroblasts serves as an autologous fibrotic brake, controlling the underlying ECM composition, structure and mechanotransduction, and suppressing fibroblast invasion and pulmonary fibrosis.

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Expression data from fibroblasts cultured from normal and fibrotic human lung tissue

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Identification and function of Tbx4 resident fibroblasts as a major source of fibrotic fibroblasts

Project description:Progressive tissue fibrosis is a major cause of morbidity, and idiopathic pulmonary fibrosis (IPF) is a terminal illness characterized by unremitting matrix deposition in the lung with very limited choice of therapies. The imcomplete understanding of the mechanisms of progressive fibrosis curbs the progress in therapeutics development. Of which, the origin of fibrotic fibroblasts has been poorly defined during the pathogenesis of tissue fibrosis. Here, we fate-mapped a early embryonic transcription factor T-box gene 4 (Tbx4)-derived mesenchymal progenitors in injured adult lung and found that Tbx4+ lineage cells are the major source of myofibroblasts. The ablation of Tbx4+ cells or disruption of Tbx4 signaling attenuated lung fibrosis in bleomycin injury model in mice in vivo. Furthermore, Tbx4+ fibroblasts are more invasive and the regulation of fibroblast invasiveness by Tbx4 is through mediating hyaluronan synthase 2 (HAS2). This study identified a major mesenchymal transcription factor driving the development of fibrotic fibroblasts during lung fibrosis. Understanding the origin, signaling, and functions of these fibroblasts would prove pivotal in the development of therapeutics for patients with progressive fibrotic diseases. We used microarrays to detail the gene expression of Tbx4 and non-Tbx4 cultured fibroblasts.

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Macropinocytosis inhibition attenuates pro-fibrotic responses in lung fibroblasts and pulmonary fibrosis

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Cysteine oxidation triggers amyloid fibril formation of the tumor suppressor p16INK4A

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Wilms’ tumor 1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions

Project description:Idiopathic pulmonary fibrosis (IPF) is a fatal fibrotic lung disease characterized by impaired fibroblast clearance, accumulation, and excessive extracellular matrix (ECM) protein production. Wilms' Tumor 1 (WT1), a transcription factor, is selectively upregulated in IPF fibroblasts. However, the mechanisms by which WT1 contributes to fibroblast accumulation and ECM production remain unknown. Here, we investigated the heterogeneity of WT1-expressing fibroblasts using single-nucleus RNA sequencing on the distal lung tissues of IPF patients and healthy controls. WT1 was selectively upregulated in a subset of IPF fibroblasts that co-expressed several pro-survival genes. Both the loss-of-function and gain-of-function studies support the idea that WT1 functions as a positive regulator of multiple pro-survival genes to impair apoptotic clearance and promote ECM production. In support, fibroblast-specific overexpression of WT1 augmented fibroproliferation, myofibroblast accumulation, and ECM production during bleomycin-induced pulmonary fibrosis in both young and old mice. Together, these findings identify WT1 as a potential therapeutic target to attenuate fibroblast expansion, and ECM production in the distal areas of fibrosing lungs.

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