Aquaporin‐3 Expression in Human Fetal Airway Epithelial Progenitor Cells

Avril-Delplanque, Aurélie; Casal, Ibrahim; Castillon, Nicolas; Hinnrasky, Jocelyne; Puchelle, Édith; Péault, Bruno

doi:10.1634/stemcells.2004-0197

Cited by 61 publications

(38 citation statements)

References 48 publications

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“…Some suggest that both populations can restore the tracheal epithelium equally well (Avril-Delplanque et al, 2005;Liu et al, 1994). However, others have found that only columnar cells (Johnson and Hubbs, 1990) or only basal cells (Ford and Terzaghi-Howe, 1992) can restore all of the epithelial cell types.…”

Section: Box 2 Transdifferentiationmentioning

confidence: 99%

Epithelial stem cells of the lung: privileged few or opportunities for many?

2006

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Most reviews of adult stem cells focus on the relatively undifferentiated cells dedicated to the renewal of rapidly proliferating tissues, such as the skin, gut and blood. By contrast, there is mounting evidence that organs and tissues such as the liver and pancreatic islets, which turn over more slowly,use alternative strategies, including the self-renewal of differentiated cells. The response of these organs to injury may also reveal the potential of differentiated cells to act as stem cells. The lung shows both slow turnover and rapid repair. New experimental approaches, including those based on studies of embryonic development, are needed to identify putative lung stem cells and strategies of lung homeostasis and repair.

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Section: Box 2 Transdifferentiationmentioning

confidence: 99%

Epithelial stem cells of the lung: privileged few or opportunities for many?

2006

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“…In vivo and in vitro studies show that epithelial repair is rapid and dynamic, involving epithelial dedifferentiation, cytoskeletal rearrangement, migration, and redifferentiation (e.g., see References 54-56). Indeed, both basal and columnar cell types reconstituted a complete epithelium in an in vivo model of rat tracheas denuded of their own cells and implanted in immune compatible hosts (57,58). However, colony formation on plastic dishes (59) and lineage tracing studies (60), as well as more recent analysis of clonal growth (61) and genetic lineage mapping (62,63), suggest that mouse tracheal basal cells have enhanced ability to form large differentiated epithelial colonies.…”

Section: Adult Lung Epithelial Stem Cellsmentioning

confidence: 99%

Airway Epithelial Stem Cells and the Pathophysiology of Chronic Obstructive Pulmonary Disease

Randell

2006

Proceedings of the American Thoracic Society

121

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Characteristic pathologic changes in chronic obstructive pulmonary disease (COPD) include an increased fractional volume of bronchiolar epithelial cells, fibrous thickening of the airway wall, and luminal inflammatory mucus exudates, which are positively correlated with airflow limitation and disease severity. The mechanisms driving general epithelial expansion, mucous secretory cell hyperplasia, and mucus accumulation must relate to the effects of initial toxic exposures on patterns of epithelial stem and progenitor cell proliferation and differentiation, eventually resulting in a self-perpetuating, and difficult to reverse, cycle of injury and repair. In this review, current concepts in stem cell biology and progenitor-progeny relationships related to COPD are discussed, focusing on the factors, pathways, and mechanisms leading to mucous secretory cell hyperplasia and mucus accumulation in the airways. A better understanding of alterations in airway epithelial phenotype in COPD will provide a logical basis for novel therapeutic approaches.Keywords: epithelium; hyperplasia; metaplasia; mucus hypersecretion; stem cellsThe human and societal toll of chronic obstructive pulmonary disease (COPD) is considerable, and there is a clear need for better prevention and early detection/intervention, including more specific and effective therapies for all stages of the disease. COPD is characterized by, and defined as, sustained and largely irreversible airflow limitation on forced exhalation, associated with known risk factors and excluding other specific causes (1, 2). The key pathologic changes underlying the physiologic hallmarks are loss of lung elasticity and small airway tethers due to emphysema, thickening of the small airway wall to reduce caliber, and luminal obstruction with inflammatory mucoid secretions (3-5). The airway epithelium is a primary interface with the outside world and is a target of the toxic particles and gases from tobacco smoke and other environmental agents that are the main cause of COPD. As indicated by changes in gene expression, airway epithelial cells respond dynamically to the inciting stimuli (6) and are the focus of viral (7) and bacterial (8-10) infections that exacerbate COPD and accelerate deterioration of lung function. The characteristic pathologic changes in the airway epithelium (Figures 1 and 2) are integral to the initiation and progression of COPD. Generalized epithelial hyperplasia, mucous secretory cell hyperplasia, squamous metaplasia, and mucus accumulation must result from disruptions in normal cell and tissue dynamics caused by both the initial stimuli and the spiral of infectious complications. Locations of stem cells, patterns of cell migration/differentiation, and the regulatory mecha-

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“…Consequently, viable respiratory BCs cannot be isolated on the basis of K expression. To overcome this issue, several groups identified cell-surface markers that can be used to separate BCs into subsets, using a fluorescence-activated cell sorter (FACS) (2,3,(8)(9)(10). One of these markers, tissue factor (TF), is a component of the extrinsic coagulation cascade (11), and was originally developed for the isolation of nasal polyp BCs (12).…”

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confidence: 99%

Human Tracheobronchial Basal Cells. Normal versus Remodeling/Repairing PhenotypesIn VivoandIn Vitro

Ghosh¹,

Ahmad²,

Jian³

et al. 2013

Am J Respir Cell Mol Biol

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Human tracheobronchial epithelial (TBE) basal cells (BCs) function as progenitors in normal tissue. However, mechanistic studies are typically performed in vitro and frequently use BCs recovered from patients who die of nonrespiratory disease. It is not knownwhether the cadaveric epithelium (1) is undergoing homeostatic remodeling and/or repair, or (2) yields BC clones that represent homeostatic processes identifiedin tissue. We sought to compare the phenotype of TBE-BCs with that of BCs cultured under optimal clone-forming conditions. TBE pathology was evaluated using quantitative histomorphometry. The cultured BC phenotype was determined by fluorescence-activated cell sorter analysis. Clone organization and cell phenotype were determined by immunostaining. The cadaveric TBE is 20% normal. In these regions, BCs are keratin (K)-5 1 and tetraspanin CD1511 , and demonstrate a low mitotic index. In contrast, 80% of the cadaveric TBE exhibits homeostatic remodeling/repair processes. In these regions, BCs are K5 1 /K15 1 /K14 1 on Recovery Days 3-13 (5). These injury/repair studies suggested that the human BC phenotype may also vary as a function of tissue homeostasis or wounding. Our primary aim involved determining the K5/K14 profile of human TBE BCs.Keratins are cytoplasmic proteins (6, 7). Consequently, viable respiratory BCs cannot be isolated on the basis of K expression. To overcome this issue, several groups identified cell-surface markers that can be used to separate BCs into subsets, using a fluorescence-activated cell sorter (FACS) (2,3,(8)(9)(10). One of these markers, tissue factor (TF), is a component of the extrinsic coagulation cascade (11), and was originally developed for the isolation of nasal polyp BCs (12). We showed that all Passage 1 TBE BCs that were cultured in bronchial epithelial cell growth medium (BEGM) were TF 1 , and that TF activity was necessary for BC survival in vitro (13). Other TBE BC markers include nerve growth factor receptor (2), podoplanin (14), CD49f (a6 integrin) (8), the tetraspanin CD151 1 (12), and Trp63 (p63) (15). Our secondary aim involved determining whether TF and CD151 were (1) expressed by TBE BCs, and (2) could be used to identify TBE BC subsets.Our previous studies and those of others indicate that TBE repair in mice is mediated by BCs that proliferate and then differentiate to replace ciliated and secretory cell types (2,5,8,14,(16)(17)(18)(19). Human BC progenitor functions can also be evaluated in vitro (20). However, most analyses of human BCs have focused on the BC population as a whole, rather than on the CLINICAL RELEVANCEHuman basal cells (BCs) function as progenitors for tracheobronchial epithelial repair and regeneration. However, the mechanisms regulating BC function are typically evaluated in vitro. The impact of these mechanistic studies is limited by a lack of cross-referencing in tissue and cultured BC phenotype and function. We show that human tracheobronchial BC phenotypes are heterogeneous in vivo, and become more homogeneous in vitro. Highly ...

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Aquaporin‐3 Expression in Human Fetal Airway Epithelial Progenitor Cells

Cited by 61 publications

References 48 publications

Epithelial stem cells of the lung: privileged few or opportunities for many?

Epithelial stem cells of the lung: privileged few or opportunities for many?

Airway Epithelial Stem Cells and the Pathophysiology of Chronic Obstructive Pulmonary Disease

Human Tracheobronchial Basal Cells. Normal versus Remodeling/Repairing PhenotypesIn VivoandIn Vitro

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