Pathogenic Stem Cell Variation in Chronic Lung Disease
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ABSTRACT:
PROVIDER: PRJNA487492 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Chronic obstructive lung disease is the third leading cause of death in the United States. We have identified and cloned the stem cell variants from patients lung samples using our cloning method. These stem cells functions are explored using combinations of microarray, single cell RNA-seq, ChIP-seq and in vivo assays.
2020-04-15 | GSE118950 | GEO
Project description:Proteolethargy is a pathogenic mechanism in chronic disease
| PRJNA1142944 | ENA
Project description:The pathogenic mechanisms of many diseases are well understood at the molecular level, but there are prevalent syndromes associated with pathogenic signaling, such as diabetes and chronic inflammation, where our understanding is more limited. Here we report that pathogenic signaling suppresses the mobility of a spectrum of proteins that play essential roles in cellular functions known to be dysregulated in these chronic diseases. The reduced protein mobility, which we call proteolethargy, was linked to cysteine residues in the affected proteins and signaling-related increases in excess reactive oxygen species. Diverse pathogenic stimuli, including hyperglycemia, dyslipidemia and inflammation, produce similar reduced protein mobility phenotypes. We propose that proteolethargy is an overlooked cellular mechanism that may account for various pathogenic features of diverse chronic diseases.
2025-01-15 | GSE273733 | GEO
Project description:These subjects were diagnosed as being controls or having interstitial lung disease (ILD) or chronic obstructive pulmonary disease (COPD) as determined by clinical history, CT scan, and surgical pathology. There was no intervention, these are cross-sectional data. All samples are from the Lung Tissue Research Consortium (LTRC) and are indexed by their LTRC tissue label. These are 319 total subjects, 183 have ILD and 136 have COPD, who went for surgery for the investigation of a nodule and have no chronic lung disease by CT or pathology. Each sample is total RNA extracted from flash frozen human whole lung homogenate. Between the two platforms were analyzed. Samples are titled by source (LT=LTRC), 6-digit tissue label, lobe of extraction, and major disease state.
2015-09-18 | E-GEOD-72967 | biostudies-arrayexpress
Project description:Identifying protein biomarkers for chronic obstructive pulmonary disease (COPD) has been challenging. Most previous studies have utilized individual proteins or pre-selected protein panels measured in blood samples. To identify COPD protein biomarkers by applying comprehensive mass spectrometry proteomics in lung tissue samples. We utilized mass spectrometry proteomic approaches to identify protein biomarkers from 152 lung tissue samples representing COPD cases and controls.
2022-01-07 | PXD024124 | Pride
Project description:<p>The pathogenic mechanisms of many diseases are well understood at the molecular level, but there are prevalent diseases associated with pathogenic signaling, such as diabetes and chronic inflammatory disorders, where our understanding is more limited. Here we report that pathogenic signaling suppresses the mobility of a spectrum of proteins that play essential roles in cellular functions known to be dysregulated in these chronic diseases. This behavior was linked to cysteine residues in the affected proteins and signaling-related increases in excess reactive oxygen species. Diverse pathogenic stimuli, including hyperglycemia, dyslipidemia and inflammation, produce similar suppressed protein mobility phenotypes. We propose that suppressed protein mobility may account for various pathogenic features of diverse chronic diseases.</p>
2024-08-09 | MTBLS9535 | MetaboLights
Project description:These subjects were diagnosed as being controls or having interstitial lung disease (ILD) or chronic obstructive pulmonary disease (COPD) as determined by clinical history, CT scan, and surgical pathology. There was no intervention, these are cross-sectional data. All samples are from the Lung Tissue Research Consortium (LTRC) and are indexed by their LTRC tissue label.
2015-09-18 | GSE72967 | GEO
Project description:Microarray data from total RNA extracted from whole lung homogenate from subjects undergoing thoracic surgery. These subjects were diagnosed as being controls or having interstitial lung disease or COPD as determined by clinical history, CT scan, and surgical pathology. There was no intervention, these are cross-sectional data. All samples are from the Lung Tissue Research Consorium (LTRC and are indexed by their LTRC tissue label). These are 582 total subjects, 254 have interstitial lung disease, 220 have COPD, and 108 are controls, who went for surgery for the investigation of a nodule and have no chronic lung disease by CT or pathology. Due to the number of samples, multipe batches of arrays were necessary, so 10% of the arrays were picked at random to have replicates throughout each batch to account for possible batch effects. The feature extracted data was normalized using a pairwise cyclic loess approach, and the probes were collapsed to one probe per gene by selecting the probe with the highest average signal. Each sample is total RNA extracted from flash frozen human whole lung homogenate. Between the two platforms were analyzed. Samples are titled by source (LT=LTRC), 6-digit tissue label, lobe of extraction, and major disease state)
2013-05-30 | E-GEOD-47460 | biostudies-arrayexpress
Project description:Tissue-resident memory T (TRM) cells are crucial mediators of adaptive immunity in non-lymphoid tissues. However, the functional heterogeneity and pathogenic roles of CD4+ TRM cells that reside within chronic inflammatory lesions remain unknown. We found that CD69hiCD103low CD4+ TRM cells produced effector cytokines and promoted the inflammation and fibrotic responses induced by chronic exposure to Aspergillus fumigatus. Simultaneously, immunosuppressive CD69hiCD103hiFoxp3+ CD4+ regulatory T (Treg) cells were induced and constrained the ability of pathogenic CD103low TRM cells to cause fibrosis. Thus, lung tissue-resident CD4+ T cells play crucial roles in the pathology of chronic lung inflammation, and CD103 expression defines pathogenic effector and immunosuppressive tissue-resident cell subpopulations in the inflamed lung.
2020-06-30 | GSE133399 | GEO
Project description:<p>Progressive decline in lung function is a hallmark of chronic obstructive pulmonary disease (COPD). Although airway dysbiosis occurs in COPD, whether it contributes to disease progression remains unknown. Here, through a longitudinal analysis on 181 COPD individuals from two large cohorts involving four UK clinical centers, we showed that baseline airway dysbiosis, characterized by enrichment of opportunistic pathogenic taxa, was associated with rapid forced expiratory volume in one second (FEV1) decline over two years. Co-presence of Moraxella, Staphylococcus and Stenotrophomonas was associated with an accelerated FEV1 decline by 139.7 mL/year. The dysbiosis was associated with exacerbation-related FEV1 fall and sudden FEV1 fall at clinical stability, two critical events contributing to long-term FEV1 decline. The microbiota association with FEV1 decline was validated in a third, independent cohort in China. Human multi-omics, murine and cellular mechanistic studies showed that chronic airway colonization of Staphylococcus aureus promoted lung function decline through producing homocysteine, which elicited an apoptosis-to-NETosis shift in neutrophils toward persistent inflammation via AKT1-S100A8/A9 axis. Prophylactic and therapeutic depletion of S. aureus via bacteriophage restored lung function in emphysema mice. These results provide a fresh approach to slow COPD progression by targeting the airway microbiome.</p><p><br></p><p><strong>Linked studies:</strong></p><p><strong>UPLC-MS/MS assays</strong> of human samples are reported in this study.</p><p><strong>UPLC-MS/MS assays</strong> of murine samples are reported in<strong> </strong><a href='https://www.ebi.ac.uk/metabolights/MTBLS6894' rel='noopener noreferrer' target='_blank'><strong>MTBLS6894</strong></a>.</p><p><strong>UPLC-MS/MS assays</strong> of original cohort human samples are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4017' rel='noopener noreferrer' target='_blank'><strong>MTBLS4017</strong></a>.</p>
2023-06-12 | MTBLS5423 | MetaboLights