Increasing evidence provide support that the mammalian liver contains stem/progenitor cells, but their molecular phenotype, embryological derivation, cell biology as well as of their role in the liver cell turnover and regeneration remain to be further clarified.
Isolation and characterization of a murine resident liver stem cell.
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Up-regulation of expression of the ubiquitin carboxyl-terminal hydrolase L1 gene in human airway epithelium of cigarette smokers.
Sex, Age, Race
View SamplesBackground: Whereas cilia damage and reduced cilia beat frequency have been implicated as causative of reduced mucociliary clearance in smokers, theoretically mucociliary clearance could also be affected by cilia length. Based on models of mucociliary clearance predicting cilia length must exceed the 6 -7 m airway surface fluid depth to generate force in the mucus layer, we hypothesized cilia height may be decreased in airway epithelium of normal smokers compared to nonsmokers.
Smoking is associated with shortened airway cilia.
Sex, Age
View SamplesUpregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers
Up-regulation of expression of the ubiquitin carboxyl-terminal hydrolase L1 gene in human airway epithelium of cigarette smokers.
Sex, Age
View SamplesResponses of the Human Airway Epithelium Transcriptome to In Vivo Injury
Responses of the human airway epithelium transcriptome to in vivo injury.
Sex, Age, Time
View SamplesModification of Gene Expression of the Small Airway Epithelium in Response to Cigarette Smoking
Modification of gene expression of the small airway epithelium in response to cigarette smoking.
Sex, Age
View SamplesAirway remodelling in chronic obstructive pulmonary disease (COPD) originates, in part, from smoking-induced changes in airway basal stem/progenitor cells (BCs). Based on the knowledge that bone morphogenetic protein 4 (BMP4) influences epithelial progenitor function in the developing and adult mouse lung, we hypothesised that BMP4 signalling may regulate the biology of adult human airway BCs relevant to COPD.
Expression of the SARS-CoV-2 ACE2 Receptor in the Human Airway Epithelium.
Specimen part
View SamplesBackground: High mobility group AT-hook1 (HMGA1) is essential for airway basal cell mucociliary differentiation, barrier integrity and wound repair. HMGA1 expression suppresses the abnormal basal cell differentiation to squamous, inflammatory and epithelial-mesenchymal transition phenotype commonly observed in association with cigarette smoking and chronic obstructive pulmonary disease (COPD). Results: HMGA1 knockdown experiments indicate that when HMGA1 expression is suppressed, the airway basal cells cannot normally differentiate into a mucociliary epithelium, form an intact barrier, and repair following injury. Instead, airway basal cell differentiation was skewed to an abnormal squamous EMT-like phenotype associated with airway remodeling in COPD. This study demonstrates that HMGA1 plays a key role in normal airway differentiation, regeneration of the normal airway epithelium following injury, and suppression of expression of genes related to squamous metaplasia, EMT and inflammation. Overall design: [RNA-seq] Non-smoker large airway epithelium cells, large airway basal cells, small airway epithelial cells, small airway basal cells. Smoker large airway basal cells, COPD smoker large airway basal cells,.
Mandatory role of HMGA1 in human airway epithelial normal differentiation and post-injury regeneration.
Specimen part, Subject
View SamplesHuman infection with Cryptococcus neoformans (Cn), a prevalent fungal pathogen, occurs by inhalation and deposition in the lung alveoli of infectious particles. The subsequent host pathogen interaction is multifactorial and can result either in eradication, latency or extra-pulmonary dissemination. Successful control of Cn infection is dependent on host macrophages as shown by numerous studies. However in vitro macrophages display little ability to kill Cn. Recently, we reported that ingestion of Cn by macrophages induces early cell cycle progression that is subsequently followed by mitotic arrest, an event that almost certainly reflects damage to the host cell. The goal of the present work was to understand macrophage pathways affected by Cn toxicity. Infection of J774.16 macrophage-like cell line macrophages by Cn in vitro was associated with changes in gene pattern expression. Concomitantly we observed depolarization of macrophage mitochondria and alterations in protein translation rate. Our results indicate that Cn infection impairs multiple host cellular functions. Therefore we conclude Cn intracellular residence in macrophages undermines the health of these critical phagocytic cells interfering with their ability to clear the fungal pathogen.
Macrophage mitochondrial and stress response to ingestion of Cryptococcus neoformans.
Specimen part, Cell line, Time
View SamplesThe pathology of chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and the majority of lung cancers involve the small airway epithelium (SAE), the single continuous layer of cells lining the airways ?6th generations. The basal cells (BC) are the stem/progenitor cells of the SAE, responsible for the differentiation into intermediate cells and ciliated, club and mucous differentiated cells. To facilitate the study of the biology of the human SAE in health and disease, we immortalized and characterized a normal human SAE basal cell line.
Characterization of an immortalized human small airway basal stem/progenitor cell line with airway region-specific differentiation capacity.
Sex, Age, Specimen part, Race
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