Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA151183 | ENA |
REPOSITORIES: ENA
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Project description:We performed genome-wide profiling of miRNA expression in the airway epithelial compartment in asthma to identify miRNA pathways associated with epithelial abnormalities using miRNA microarrays and real-time PCR. We also sought to identify the effect of inhaled corticosteroids (ICS) on airway epithelial miRNA expression Samples were obtained from airway epithelial cells by bronchoscopic brushing from three groups of subjects: Healthy Controls ( N=12), Steroid Naïve Asthma (N=16), Steroid-requiring Asthma (N=19).
2012-12-05 | E-GEOD-34466 | biostudies-arrayexpress
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Project description:Airway inflammation is the hallmark of asthma and suggests a dysregulation of homeostatic mechanisms. MicroRNAs (miRNAs) are key regulators of gene expression, necessary for the proper function of cellular processes. We used miRNA microarrays to compare the profiles of human bronchial epithelial cells from healthy and asthmatic donors
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Project description:Airway inflammation is the hallmark of asthma and suggests a dysregulation of homeostatic mechanisms. MicroRNAs (miRNAs) are key regulators of gene expression, necessary for the proper function of cellular processes. We used miRNA microarrays to compare the profiles of human bronchial epithelial cells from healthy and asthmatic donors Human bronchial epithelial cells were isolated from healthy and asthmatic donors. RNA was extracted and miRNA expression was analyzed on Affymetrix miRNA microarrays. We sought to utilize miRNA expression as a tool for understanding underlying biological differences in BECs from healthy and asthmatic donors.
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Project description:Recent evidence suggests that bronchial epithelial cells from asthmatic patients exhibit altered metabolic signatures. This metabolic shift of energetically demanding cells leads to increased inflammation, excessive reactive oxygen species production (ROS), and oxidative stress—all hallmarks of mitochondrial dysfunction. While mitochondrial dysfunction has been implicated in asthmatic epithelial cells, the mechanistic link between bronchoconstriction and these metabolic alterations remains poorly defined. Club cell secretory protein (CC16) is the most abundant protein found in the lung and exerts key anti-inflammatory and antioxidant functions, culminating in protection against airway remodeling. Decreased levels of CC16 are characteristic of asthma and worsening respiratory disease. Using a well-established transmembrane compression system to model bronchoconstriction coupled with mass spectrometry and quantitative proteomics, we investigated how modeling bronchoconstriction in airway cells impacts CC16 expression and cell metabolic pathway changes over time. Additionally, using rCC16, we examined the direct impact on airway cell metabolism. Using naïve mouse tracheal epithelial cells (MTECs) and normal human bronchial epithelial cells (HBECs), we observed that rCC16 induces the expression of proteins related to various metabolic pathways, such as glycolysis, gluconeogenesis, and the pentose phosphate pathway and that compression of airway cells results in acute decreases in CC16 expression, as well as decreases in metabolic processes. MTECs deficient in CC16 (CC16-/-) had lower mitochondrial oxygen consumption rate (OCR) compared to WT cells, both of which could be increased by exogenous addition of rCC16. Our findings suggest a novel role for CC16 in mediating airway epithelial cell metabolic processes, which could be decreased by bronchoconstrictive events in asthma patients.
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