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Charaterization of function of ST2 receptor on macrophages function during Club cell regeneration after naphthalene injury in WT mice

ABSTRACT: Charaterization of function of ST2 receptor on macrophages function during Club cell regeneration after naphthalene injury in WT mice

PROVIDER: PRJNA649519 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12344113_1.fastq.gz	Fastqsanger.gz
	SRR12344113_2.fastq.gz	Fastqsanger.gz
	SRR12344114_1.fastq.gz	Fastqsanger.gz
	SRR12344114_2.fastq.gz	Fastqsanger.gz
	SRR12344115_1.fastq.gz	Fastqsanger.gz

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Charaterization of function of ST2 receptor on macrophages function during Club cell regeneration after naphthalene injury in WT mice

Project description:During repair phase after naphathalene injury 3 subsets of myeloid cells accumulate at the site of injury including P1 (monoyte), P2 (monocyte-derived macrophages and P3 (resident alternatively activated airway macrophages). ST2 receptor was found to be expressed by P2 and P3 subsets. To understand which biological processes in lung macrophages were regulated by ST2, myeloid cell subsets were flow-sorted from Naphthalene-treated WT and ST2-/- mice on d6 and their transcriptome analyzed using RNA-seq

2020-07-30 | GSE155359 | GEO

Charaterization of monocytes/macrophages function in Club cell regeneration after naphthalene injury in WT mice

Project description:Charaterization of monocytes/macrophages function in Club cell regeneration after naphthalene injury in WT mice

| PRJNA649517 | ENA

Bronchiolar progenitors and club cells in mouse lung

Project description:Gene expression patterns of bronchiolar progenitors and club cells in mouse lung were examined by microarray experiments. Although it has not yet been fully characterized, a subset of epithelial cells lining bronchioles are best understood as bronchiolar progenitors that self-renew over the long term and that can differentiate into more differentiated club cells and ciliated cells. The bronchiolar progenitors are distinct from club cells and characteristically express the alveolar type 2 cell marker, prosurfactant protein C, with lower levels of club cell secretory protein/Scgb1a1. There are also functional differences between them; while club cells can be depleted by naphthalene because of the abundance of cytochrome P450 enzyme Cyp2f2, bronchiolar progenitors are resistant to naphthalene-induced depletion because of defects in the enzyme.

2016-02-17 | E-MTAB-4460 | biostudies-arrayexpress

Depletion of club cells attenuates bleomycin-induced lung injury and fibrosis in mice

Project description:Background and objective: The role of bronchiolar epithelial cells in the pathogenesis of pulmonary fibrosis has not been addressed. We previously demonstrated that DNA damage was found in bronchiole at early phase, and subsequently extended to alveolar cells at later phase in bleomycin-induced pulmonary fibrosis in mice. Club cells are progenitor cells for bronchiole, and are recognized to play protective roles against lung inflammation and damage. The aim of the study was to elucidate the role of club cells in the development of pulmonary fibrosis. Methods: C57BL/6J mice were received naphthalene intraperitoneally at day -2 to deplete club cells, and were given intratracheal bleomycin or vehicle at day 0. Lung tissues were obtained at day 1, 7, and 14, and bronchoalveolar lavage was performed at day 14. Gene expression was analysed from bronchiolar ephithelial cells sampled by laser captured microdissection at day 14. Results: Surprisingly, naphthalene-induced club cell depletion protected mice from bleomycin-induced lung injury and fibrosis. We conclude that club cells are involved in the development of lung injury and fibrosis.

2017-02-08 | GSE94522 | GEO

Club cells employ regeneration mechanisms during lung tumorigenesis

Project description:Lung adenocarcinoma (LUAD) is one of the deadliest malignancies worldwide. Dynamic lineage changes within the lung epithelium and the high plasticity of these epithelial cells confound the correct identification of the cell-of-origin of LUAD. Here, we combined lineage-tracing mouse models with an autochthonous cell type-independent LUAD model in order to discover the cellular origin of ALK-translocated LUAD. We identified Club and AT2 cells as the cells-of-origin of LUAD. Moreover, we uncovered epigenetic imprints in the tumours originating from Club or AT2 cells by whole-genome bisulfite sequencing. Single-cell transcriptomes of Club cells at different stages of tumour development identified two trajectories of Club cell evolution. On both routes, tumours lose their Club cell identity and gain an AT2-like phenotype. Together, this study highlights the role of Club cells in LUAD initiation and unveils key mechanisms conferring LUAD heterogeneity.

2022-06-30 | GSE176185 | GEO

Club cells employ regeneration mechanisms during lung tumorigenesis

2022-06-30 | GSE176184 | GEO

IL-33-ST2 axis regulates myeloid cell differentiation and activation facilitating effective club cell regeneration

Project description:IL-33-ST2 axis regulates myeloid cell differentiation and activation facilitating effective club cell regeneration

| PRJNA649522 | ENA

Involvement of Igf1r in Bronchiolar Epithelial Regeneration: Role During Repair Kinetics after Selective Club Cell Ablation

Project description:Regeneration of lung epithelium is vital for maintaining airway function and integrity. An imbalance between epithelial damage and repair is at the basis of numerous chronic lung diseases such as asthma, COPD, pulmonary fibrosis and lung cancer. IGF (Insulin-like Growth Factors) signaling has been associated with most of these respiratory pathologies, although their mechanisms of action in this tissue remain poorly understood. Expression profiles analyses of IGF system genes performed in mouse lung support their functional implication in pulmonary ontogeny. Immuno-localization revealed high expression levels of Igf1r (Insulin-like Growth Factor 1 Receptor) in lung epithelial cells, alveolar macrophages and smooth muscle. To further understand the role of Igf1r in pulmonary homeostasis, two distinct lung epithelial-specific Igf1r mutant mice were generated and studied. The lack of Igf1r disturbed airway epithelial differentiation in adult mice revealed enhanced proliferation and altered morphology in distal airway club cells. During recovery after naphthalene-induced club cell injury, the kinetics of terminal bronchiolar epithelium regeneration was hindered in Igf1r mutants, revealing increased proliferation and delayed differentiation of club and ciliated cells. Amid airway restoration, lungs of Igf1r deficient mice showed increased levels of Igf1, Insr, Igfbp3 and epithelial precursor markers, reduced amounts of Scgb1a1 protein, and alterations in IGF signaling mediators. These results support the role of Igf1r in controlling the kinetics of cell proliferation and differentiation during pulmonary airway epithelial regeneration after injury.

2017-02-09 | GSE88836 | GEO

Pairwise comparison of ST2+ and ST2- FOXP3+ T cells derived from mouse intestinal tumors

Project description:Colorectal cancer (CRC) was induced in Foxp3/eGFP reporter mice by the azoxymethane/dextran sulphate sodium salt (AOM/DSS) protocol. Mice were injected i.p. with the procarcinogen AOM (12.5 mg/kg of body weight). After 1 week, mice received drinking water supplemented with 2.5% DSS for 5 to 7 days, followed by 2 weeks of regular water. The DSS administration was repeated twice with 2% DSS. Mice were sacrificed at week 11 and lamina propia lymphocytes (LPLs) from the colon were isolated. CD4+FOXP3+ (eGFP+) ST2+ or ST2- Tregs were separated from colonic LPLs of CRC induced mice using a FACSAria II cell sorter. Microarray analysis was performed to analyze if ST2+ FOXP3+ Tregs from the colon of CRC mice present a distinct transcription pattern compared to ST2- FOXP3+ Tregs. By this, the role of ST2 for Treg function during intestinal tumorigenesis should be characterized.

2019-05-31 | E-MTAB-6842 | biostudies-arrayexpress

ST2+ T-regulatory Cells in Renal Inflammation and Fibrosis following Ischemic Kidney Injury

Project description:The role of IL-33 and its receptor ST2 in kidney injury is not well understood. This study demonstrates the importance of ST2 expression on the T-regulatory cells (Tregs) for the resolution of renal injury by suppressing inflammation and fibrosis. Treg-specific deletion of ST2, detrimentally impacted late outcomes of renal injury worsening the impairment of kidney function, inflammation, and fibrosis.

2024-08-27 | GSE272380 | GEO

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