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Transcriptome mapping of alveolar macrophages developing under Scgb1a1 deficiency.

ABSTRACT: Transcriptome mapping of alveolar macrophages developing under Scgb1a1 deficiency.

PROVIDER: PRJNA625292 | ENA |

REPOSITORIES: ENA

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Transcriptome mapping of alveolar macrophages developing under Scgb1a1 deficiency.

Project description:Alveolar macrophage (AM) is a mononuclear phagocyte key to the defense against respiratory infections. To understand AM’s role in airway disease development, we examined the influence of Secretoglobin family 1a member 1 (SCGB1A1), a pulmonary surfactant protein, on AM development and function. In a murine model, high-throughput RNA-sequencing and gene expression analyses were performed on purified AMs isolated from mice lacking in Scgb1a1 gene and were compared with that from mice expressing wild type Scgb1a1 at weaning (4wk), puberty (8wk), early adult (12wk) and middle age (40wk). AMs from early adult mice under Scgb1a1 sufficiency demonstrated a total of 37 upregulated biological pathways compared to that at weaning, from which 30 were directly involved with antigen presentation, anti-viral immunity and inflammation. Importantly, these pathways under Scgb1a1 deficiency were significantly downregulated compared to that in the age-matched Scgb1a1-sufficient counterparts. Furthermore, AMs from Scgb1a1-deficient mice showed an early activation of inflammatory pathways compared with that from Scgb1a1-sufficient mice. Our in vitro experiments with AM culture established that exogenous supplementation of SCGB1a1 protein significantly reduced AM responses to microbial stimuli where SCGB1a1 was effective in blunting the release of cytokines and chemokines (including IL-1b, IL-6, IL-8, MIP-1a, TNF-a and MCP-1). Taken together, these findings suggest an important role for Scgb1a1 in shaping AM-mediated inflammation and immune responses, and in mitigating cytokine surges in the lungs.

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Gene expression profiling of Scgb1a1+, CD24low cells isolated from the lungs of Scgb1a1-CreER; Rosa26-mTmG mouse.

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Lung Secretoglobin Scgb1a1 Influences Alveolar Macrophage-Mediated Inflammation and Immunity.

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Radiation-activated secretome of Scgb1a1+ club cells increase the efficacy of immune checkpoint blockade in lung cancer (Bulk048 RNA-seq)

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RNA-seq analysis of RNA extracted from control alveolar bone samples and alveolar bone under apical periodontitis

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Alveolar Injury and Regeneration Following Deletion of ABCA3

Project description:Surfactant deficiency, diffuse alveolar damage and respiratory failure caused by loss of Abca3 in AT2 cells was followed by remarkable proliferation of alveolar cells and selective survival of ABCA3 sufficient cells resulting in regeneration of alveolar structure and function, providing the conceptual framework for the development of therapies to ameliorate lung diseases caused by mutations in ABCA3 and other genes critical for AT2 cell function or surfactant homeostasis.

2018-02-15 | GSE103506 | GEO

Profiling AT1 and AT2 cells throughout alveolar development

Project description:This experiment profiled the transcriptomes of developing AT1 and AT2 cells from the beginning of embryonic alveolar development through the end of alveologenesis at 6 weeks of age.

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Differential impact of Dicer deficiency on microglia of the developing and adult brain

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Insights into pulmonary phosphate homeostasis and osteoclastogenesis emerge from the study of pulmonary alveolar microlithiasis

Project description:Pulmonary alveolar microlithiasis is an autosomal recessive lung disease caused by a deficiency in the pulmonary epithelial Npt2b sodium-phosphate co-transporter that results in accumulation of phosphate and formation of hydroxyapatite microliths in the alveolar space. The single cell transcriptomic analysis of a pulmonary alveolar microlithiasis lung explant showing a robust osteoclast gene signature in alveolar monocytes and the finding that calcium phosphate microliths contain a rich protein and lipid matrix that includes bone resorbing osteoclast enzymes and other proteins suggested a role for osteoclast-like cells in the host response to microliths. While investigating the mechanisms of microlith clearance, we found that Npt2b modulates pulmonary phosphate homeostasis through effects on alternative phosphate transporter activity and alveolar osteoprotegerin, and that microliths induce osteoclast formation and activation in a receptor activator of nuclear factor kappa B (NF-kB) ligand and dietary phosphate dependent manner. This work reveals that Npt2b and pulmonary osteoclast like cells play key roles in pulmonary homeostasis and suggest potential new therapeutic targets for the treatment of lung disease.

2023-02-16 | MSV000091302 | MassIVE

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