Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA140451 | ENA |
REPOSITORIES: ENA
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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: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: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: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:We have used microarrays to identify individual genes and pathways regulated by Gq/11 or G12/13 signalling in type II alveolar epithelial cells isolated from the lungs of knockout mice.
2016-10-25 | GSE87842 | GEO
Project description:For this project alveolar epithelial type-II cells (AT-II) were FACS sorted from 8 donor lungs and 6 fibrotic lungs. The main goals of this experiment is to identify differences in transcriptional programms in AT-II cells from human donor and IPF patients.
2021-10-12 | GSE185691 | GEO
Project description:Comparison of rat freshly-isolated alveolar epithelial type I cells, freshly-isolated type II cells, and type II cells cultured for 7 days Keywords = rat, alveolar epithelial type I cells, cultured type II cells Keywords: parallel sample
2004-11-01 | GSE1567 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) is a progressive disease that obstructs the airflow from the lungs, and tobacco smoking is the major cause of COPD. Here, we applied single-cell RNA sequencing to analyze COPD pathogenesis in COPD patients, non-COPD smokers and never-smokers and investigated the disease progression at single-cell resolution. By single-cell transcriptome analysis, we identified a novel subpopulation of Alveolar Type 2 epithelial cells that emerged in smokers, such as COPD patients, and specifically expressed a series of chemokines and PD-L1. Since the number of cells in the basal cell clusters increased in only the COPD lungs but not in the non-COPD smoker or never-smoker lungs, we also tried to clarify the difference in phenotype between COPD and other basal cells with single-cell RNA-seq. However, due to the small number of cells in each, no clear difference could be found. To further investigate the functional properties of basal cells in COPD, we isolated small airway epithelial cells from surgical samples of COPD or never-smoker lungs and expanded the cells in vitro.Total RNA was extracted from early passaged cells , and bulk RNA-seq was performed to characterize these cells in detail. Finally, we found that the COPD basal cells retained the inflammatory response and basal/stem-related signals, even after a few passages in culture, and it might cause basal cell expansion in vivo.
2021-06-10 | GSE162154 | GEO
Project description:Normal lung function relies on mature function of alveolar type II cels, which have numerous functions including to regulate ion and fluid flux, produce immune molecules, and synthesize and secrete surfactant to stabilize air spaces. Differentiation of type II cells from precursor epithelial cells is accelerated by exposure of cultured cells to glucocorticoid and cAMP. In these studies we used DNA microarray analysis to identify genes of both fetal and adult type II cells that are regulated by glucocorticoid plus cAMP. In the first series of experiments we isolated epithelial cells from fetal human lung and cultured cells for 5 days with or without hormone treatment (dexamethasone plus 8-Br-cAMP plus isobutylmethylxanthine, DCI) and then performed DNA microarray analysis. In the second series of experiments, we isolated type II cells from adult human postmortem lung and cultured cells for 5 days with or without DCI and performed DNA microarray analysis.
2009-12-30 | E-GEOD-19699 | biostudies-arrayexpress
Project description:Chronic obstructive pulmonary disease (COPD) is a progressive disease that obstructs the airflow from the lungs, and tobacco smoking is the major cause of COPD. Here, we applied single-cell RNA sequencing to analyze COPD pathogenesis in COPD patients, non-COPD smokers and never-smokers and investigated the disease progression at single-cell resolution. By single-cell transcriptome analysis, COPD was characterized by shifts in the stromal, immune system and epithelial cell compositions. While epithelial components in never-smokers were relatively uniform, the smoker groups presented with extensive heterogeneity in epithelial cells, particularly in the alveolar type II (AT2) lineages. We identified a subpopulation of AT2 epithelial cells that emerged in smokers, such as COPD patients, and specifically expressed a series of chemokines and PD-L1. A trajectory analysis revealed that the inflammatory AT2 cell subpopulation followed a unique differentiation path, and a prediction model of cell-to-cell interactions inferred increased intercellular networks of inflammatory AT2 cells with immune and stromal cell populations. Thus, our analysis reveals a unique cellular differentiation pathway and function underlying the biological and clinical characteristics of COPD pathogenesis.
2021-06-29 | GSE173896 | GEO