A new approach for the study of lung smooth muscle phenotypes and its application in asthma
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE45723 | GEO | 2014/03/13
SECONDARY ACCESSION(S): PRJNA196129
REPOSITORIES: GEO
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Project description:We developed a new method for the isolation of bronchial smooth muscle cells. This method is built upon a double fluorescent mouse SMA-GFP;NG2-DsRed and cell sorting. Using this method, we isolated bronchial smooth muscle cells from control and asthmatic C57BL/6J mice for gene profiling. Double fluorescent mice were induced to develop asthma using OVA. Bronchial smooth muscle cells were purified from asthmatic and control mice for mRNA array.
2014-03-13 | E-GEOD-45723 | biostudies-arrayexpress
Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. We thus hypothesis that asthmatic BSM cells could act on bronchial epithelium and modified its response to rhinovirus infection.
2023-05-02 | PXD015604 | Pride
Project description:Bronchial Epithelial Cells were isolated processed as described (Chu et al., 2002 and Zhao et al., 2011). The objective of the study was to identify differentially expressed genes between normal control (NC), mild-moderate asthmatic (MMA) and severe asthmatic (SA) patients. Isolated fresh bronchial epithelial cells were placed into trizol for further analysis.
2014-07-01 | E-GEOD-43696 | biostudies-arrayexpress
Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. Thus, we hypothesis that asthmatic BSM cell metabolism is modified compare to that of non-asthmatic and that could be a potential target to reduce asthmatic BSM cell proliferation and remodeling in asthma.
2021-06-10 | PXD015566 | Pride
Project description:Persistent severe asthma is associated with hyper-contractile airways and structural changes in the airway wall, including an increased airway smooth muscle (ASM) mass. This study used gene expression profiles from asthmatic and healthy airway smooth muscle cells grown in culture to identify novel receptors and pathways that potentially contributed to asthma pathogenesis. We used microarrays to compare the gene expression between asthmatic and healthy airway smooth muscle cells to understand the underlying pathway contributing the differences in cellular phenotypes Asthmatic airway smooth muscle cells (ASMC) are intrinsically different and have a differential transcriptional response to pro-fibrotic, pro-proliferation and pro-inflammatory stimuli than ASMC from healthy patients. We sought to identify genes that are differentially expressed between asthmatic and healthy ASMC under various stimulations which mimic the asthmatic airways. To this end, we obtained human ASMC from bronchial biopsies and explanted lungs from doctor diagnosed asthmatic patients (n=3) and healthy controls (n=3). The ASMC were then grown in culture and treated with pro-fibrotic (Transforming growth factor beta (TGFβ)), pro-proliferation (Fetal Bovine Serum (FBS)) and pro-inflammatory stimuli (Interleukin-1 beta (IL-1β)) for 8 hours. Gene expression was then evaluated using Affymetrix Human Gene 1.0ST arrays.
2015-01-31 | E-GEOD-63383 | biostudies-arrayexpress
Project description:Bronchial Epithelial Cells were isolated processed as described (Chu et al., 2002 and Zhao et al., 2011). The objective of the study was to identify differentially expressed genes between normal control (NC), mild-moderate asthmatic (MMA) and severe asthmatic (SA) patients.
2014-07-01 | GSE43696 | GEO
Project description:Signalling pathways regulate all major cellular events in health and disease, including asthma development and progression. Complexity of human intracellular signalization can be explored using novel systemic approaches that exploit whole-transcriptome analysis. Cap-analysis-of-gene-expression (CAGE) is a method of choice for generating transcriptome libraries, as it interrogates only terminally capped mRNAs that have the highest probability to be translated into protein. In this study we for the first time systematically profiled differentially activated Intracellular Signalling Pathways (ISPs) in cultured primary human airway smooth muscle (ASM) cells from asthmatic (n=8) and non-asthmatic (n=6) subjects in a high-throughput assay, highlighting asthma-specific co-regulatory patterns. CAGE-libraries from primary human ASM cells were subject to massive parallel next generation sequencing, and a comprehensive analysis of ISP activation was performed using a recently developed technique OncoFinder. Analysis of 270 ISPs led to discovery of multiple pathways clearly distinguishing asthmatic from normal cells. In particular, we found 146 (p<0.05) and 103 (p<0.01) signalling pathways differentially active in asthmatic vs non-asthmatic samples. We identified seven clusters of coherently acting pathways functionally related to the disease. Pathways down-regulated in asthma mostly represented cell death-promoting pathways, whereas the up-regulated ones were mainly involved in cell growth and proliferation, inflammatory response and some specific reactions, including smooth muscle contraction and hypoxia - related signalization. Most of interactions uncovered in this study were not previously associated with asthma, suggesting that these results may be pivotal to development of novel therapeutic strategies that specifically address the ISP signature linked with asthma pathophysiology. Capped mRNA profiles of primary bronchial smooth muscle cells from 8 asthmatic and 6 healthy donors were generated by deep sequencing using Illumina HiSeq1500.
2016-02-17 | E-GEOD-63744 | biostudies-arrayexpress
Project description:Understanding the gene expression changes that are occuring with TGFb1 and IL-13 treatment that result in observed phenotypic changes in bronchial smooth muscle shortening/remodeling.
2023-02-01 | GSE220972 | GEO
Project description:Rationale: Augmented smooth muscle contractility of the airways is one of the causes of airway hyperresponsiveness in asthmatics. However, the mechanism of the altered properties of airway smooth muscle cells is not well understood. Objectives: To identify differentially expressed genes (DEGs) related to the bronchial smooth muscle (BSM) hyper-contractility in a murine asthma model. Methods: The ovalbumin (OA)-sensitized mice were repeatedly challenged with aerosolized OA to induce asthmatic reaction. Transcriptomic profiles were generated by microarray analysis of BSMs from the OA-challenged and control animals, and KEGG (Kyoto Encyclopedia of Genes and Genomes) Pathway Analysis was applied. Measurements and Main Results: Tension study showed a BSM hyperresponsiveness to acetylcholine (ACh) in the OA-challenged mice. A total of 770 genes were differentially expressed between the OA-challenged and control animals. Pathway analysis showed a significant change in arachidonic acid (AA) metabolism pathway in BSMs of the OA-challenged mice. Validation of DEGs by quantitative RT-PCR showed a significant increase in PLA2 group 4c (Pla2g4c)/COX-2 (Ptgs2)/PGD2 synthase 2 (Hpgds) axis. PGD2 level in bronchoalveolar fluids of the OA-challenged mice was significantly increased. A 24-h incubation of BSMs with PGD2 caused a hyperresponsiveness to ACh in naive control mice. Conclusions: AA metabolism is shifted towards PGD2 production in BSMs of asthma. Increased PGD2 level in the airways might be a cause of the BSM hyperresponsiveness in asthma.
2018-07-03 | GSE116504 | GEO
Project description:Bronchial Epithelial Cells were isolated processed as described (Chu et al., 2002 and Zhao et al., 2011). The objective of the study was to identify differentially expressed genes between normal control (NC), mild-moderate asmathic (notSA) and severe asthmatic (SA) patients. For demographics data, contact Dr.Sally Wenzel (wenzelse@upmc.edu)
2014-11-14 | GSE63142 | GEO