Bronchial Epithelial Cell Transcriptomics: A Tool to Monitor and Predict Chronic Obstructive Pulmonary Disease Progression?

Santi, Chiara De; Greene, Catherine M.

doi:10.1165/rcmb.2021-0057ed

Cited by 1 publication

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References 13 publications

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“…There is increasing evidence that disruptions in the physical structure of the epithelium are critical early changes in the development of many chronic lung diseases, including chronic obstructive pulmonary disease (COPD) 9 , 10 with transcriptomics analysis indicating a “loss of epithelial coherence,” decline of regenerative repair as the initial defects in disease pathogenesis, and early changes in expression of genes involved in the actin cytoskeleton and cell adhesion being spurring 10 . We and others have previously reported that chronic cigarette smoke (CS) exposure to primary human bronchial epithelial cells in an air-liquid interface reduces E-cadherin, and patients with COPD have less E-cadherin 4 , 11 – 15 .…”

Section: Introductionmentioning

confidence: 99%

Loss of E-cadherin is causal to pathologic changes in chronic lung disease

et al. 2022

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Epithelial cells line the lung mucosal surface and are the first line of defense against toxic exposures to environmental insults, and their integrity is critical to lung health. An early finding in the lung epithelium of patients with chronic obstructive pulmonary disease (COPD) is the loss of a key component of the adherens junction protein called E-cadherin. The cause of this decrease is not known and could be due to luminal insults or structural changes in the small airways. Irrespective, it is unknown whether the loss of E-cadherin is a marker or a driver of disease. Here we report that loss of E-cadherin is causal to the development of chronic lung disease. Using cell-type-specific promoters, we find that knockout of E-cadherin in alveolar epithelial type II but not type 1 cells in adult mouse models results in airspace enlargement. Furthermore, the knockout of E-cadherin in airway ciliated cells, but not club cells, increase airway hyperreactivity. We demonstrate that strategies to upregulate E-cadherin rescue monolayer integrity and serve as a potential therapeutic target.

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