Role of Gq/11 and G12/13 signalling in Type II alveolar epithelial cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE87842 | GEO | 2016/10/25
SECONDARY ACCESSION(S): PRJNA347839
REPOSITORIES: GEO
Similar Datasets
Project description:Role of Gq/11 and G12/13 signalling in Type II alveolar epithelial cells
| PRJNA347839 | ENA
Project description:The alveolar epithelial cells are known producers of basement membrane components of the ECM, we hypothesize that they may also contribute substantially to remodeling of interstitial ECM in the alveolar compartment in chronic lung diseases such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). Primary human alveolar type II epithelial cells (AECII) were isolated from human lungs without lung disease or with end stage COPD, using the surface marker HT2-280. Isolated cells were cryopreserved without prior expansion and then directly seeded into decellularized distal lung parenchyma from healthy human lungs. Cells were cultured for 13 days with addition of a profibrotic stimuli in the form of 2 ng/ml of TGF-ß1 at day 7, to a subgroup samples with cells derived from healthy lungs. AECII cells comes from 5 healthy cell donors and 3 with COPD, decellularized scaffolds were prepared from 5 different healthy lungs. The data set contains a total of 71 samples each representing a unique cell/scaffold/treatment combination at either day7 or day 13 of culture. For each sample there exists a matched proteomics sample from mass spectrometry analysis deposited to the ProteomeXchange Consortium via the PRIDE partner repository. The data indicate a substantial potential of alveolar epithelial cells to directly contribute to matrisome turnover and ECM remodeling in the lung.
2022-10-31 | GSE191279 | GEO
Project description:Resident stem/progenitor cells in the lung are important for tissue homeostasis and repair. However, a progenitor population for alveolar type II (ATII) cells in adult human lungs have not been identified. Here we isolated alveolar epithelial progenitor cells (AEPCs) from adult human lungs. AEPCs showed mesenchymal stem cell (MSC)-like characteristics combined with ATII cell-phenotypes. AEPCs had the capability for self-renewal and the potential to generate ATII cells in vitro. Furthermore, cells expressing similar markers were present within alveolar walls in normal lungs and these cells were significantly increased in ATII cell hyperplasias. These results suggest that adult human lungs contain a progenitor population for ATII cells.
2010-11-16 | GSE21095 | GEO
Project description:The structure of alveoli is critical for proper lung function, the extracellular matrix (ECM) that forms these delicate structures need to be maintained throughout life, when this fails, patients suffer from conditions such as emphysema or lung fibrosis. The alveolar walls are lined by alveolar epithelial cells (AEC), and we herein set out to examine their potential to contribute to ECM remodeling in a human three-dimensional in vitro model based on human lung ECM. Cryopreserved type 2 AEC (AEC2) isolated from healthy lungs and lungs of patients with chronic obstructive pulmonary disease (COPD) were cultured in decellularized human lung slices over a period of 13 days. AEC2 from healthy lungs were treated with transforming growth factor ß1 (TGF-ß1) to evaluate the plasticity of their ECM production. Evaluation of phenotypic markers and expression of matrisome genes and proteins were performed by RNA-sequencing, mass spectrometry and immunohistochemistry. AEC2 in our model displayed an AEC marker profile similar to freshly isolated AEC2. COPD-derived AEC2 retained expression of known disease markers such as HLA-A throughout the culture period. AEC2 matrisome expression was found not to be limited to basement membrane components but included a complex set of structural proteins found in interstitial ECM. With TGF-ß1 stimuli, AEC2 showed a change in ECM production resembling what have previously been documented in mesenchymal cells, without loss of AEC marker expression. A previously unexplored potential of AEC to directly contribute to ECM turnover is revealed, motivating a re-evaluation of the role of AEC2 in pathological lung remodeling.
2023-06-29 | PXD034531 | Pride
Project description:Alveolar epithelial type II (ATII) cells play a critical role in homeostasis and repair process of the lungs. In lung diseases such as chronic obstructive pulmonary disease (COPD), ATII cells are damaged and fall into apoptosis or senescence. Until to date, global gene expression of ATII cells in COPD lungs has not been analyzed. We isolated ATII cells from three non-COPD and three COPD patients using a FACS method. Then, we performed microarray analysis to compare gene expression profiles of ATII cells between non-COPD and COPD patients.
2012-10-11 | GSE29133 | GEO
Project description:Lung aging triggers the onset of various chronic lung diseases, with alveolar repair being a key focus for alleviating pulmonary conditions. The regeneration of epithelial structures, particularly the differentiation from type II alveolar epithelial (AT2) cells to type I alveolar epithelial (AT1) cells, serves as a prominent indicator of alveolar repair. Nonetheless, the precise role of aging in impeding alveolar regeneration and the underlying mechanism remain to be fully elucidated. To elucidate the mechanisms underlying AT2 cell functional decline during lung aging, we employed transcriptomic techniques to explicit the differences in gene expression between AT2 cells of young (3-month old) and old (24-month old) mouse lungs, and revealed correlation between inflammatory factors and genes regulating proliferation and differentiation. Physiological aging-induced chronic inflammation impairs AT2 cell functions, hindering tissue repair and promoting lung disease progression. This study offers novel insights into chronic inflammation's impact on stem cell-mediated alveolar regeneration.
2024-04-03 | GSE253790 | GEO
Project description:Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%. 4 never smokers and 4 active smokers were recruited for the study. After bronchoalveolar lavage and RNA isolation, gene expression was measured using Affymetrix Human Exon 1.0 ST arrays.
2012-10-02 | E-GEOD-34517 | biostudies-arrayexpress
Project description:To determine the influence of primary tumors on pre-metastatic lungs, we have employed whole genome microarray expression profiling as a discovery platform to identify gene signatures of alveolar type II epithelial cells (AT-II) in TLR3 deficient mice (Tlr3-/-) and wide-type (WT) littermates with tumor bearing. We subcutaneously inoculated Tlr3-/- and WT mice with Lewis lung carcinoma (LLC). Two weeks later, lung tissues from Tlr3-/- and WT mice were dissociated and AT-II cells were sorted. AT-II cells from mice without tumor bearing were set as controls. Primary tumor induced gene expression in AT-II cells from Tlr3-/- and WT mice was measured at 2 weeks after tumor inoculation subcutaneously. AT-II cells from mice without tumor bearing were set as controls.
2016-08-10 | E-GEOD-76397 | biostudies-arrayexpress
Project description:Pulmonary inflammation compromises lung barrier function and underlies many lung diseases including acute lung injury and acute respiratory distress syndrome (ARDS). However, mechanisms by which lung cells respond to the damage caused by the inflammatory insults are not completely understood. Here we show that Fzd6-deficiency in Foxj1+ ciliated cells reduces pulmonary permeability, lipid peroxidation, and alveolar cell death accompanied with an increase in alveolar number in lungs insulted by LPS or mouse coronavirus MHV-1. Single cell RNA sequencing of lung cells indicates that the lack of Fzd6, which is primarily expressed in Foxj1+ ciliated cells, increases expression of the aldo-keto reductase Akr1b8. Intratracheal administration of the Akr1b8 protein phenocopies Fzd6-deficient lung phenotypes. In addition, ferroptosis inhibitors also phenocopy Fzd6-deficient lung phenotypes and exert no further effects in Fzd6-deficient lungs. These results indicate that Fzd6-deficiency suppresses inflammation-induced ferroptotic death of alveolar cells via the release of Akr1b8, thus revealing a previously unknown mechanism by which Fzd6 signaling regulates ferroptosis via a paracrine pathway. In addition, this study demonstrates the yet-to-be appreciated importance of ciliated cells in protecting alveolar cells during pulmonary inflammation.
2023-01-31 | GSE222753 | GEO
Project description:Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%.
2012-10-02 | GSE34517 | GEO