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Airway basal cell injury after acute diacetyl (2,3-butanedione) vapor exposure.

Authors
  • McGraw, Matthew D1
  • Kim, So-Young2
  • Reed, Christina3
  • Hernady, Eric4
  • Rahman, Irfan4
  • Mariani, Thomas J5
  • Finkelstein, Jacob N3
  • 1 Department of Pediatrics, Division of Pulmonology, Rochester, NY, United States; Department of Environmental Medicine, Rochester, NY, United States. Electronic address: [email protected] , (United States)
  • 2 Department of Pediatrics, Division of Pulmonology, Rochester, NY, United States. , (United States)
  • 3 Department of Environmental Medicine, Rochester, NY, United States; Department of Pediatrics, Division of Neonatology, Rochester, NY, United States. , (United States)
  • 4 Department of Environmental Medicine, Rochester, NY, United States. , (United States)
  • 5 Department of Pediatrics, Division of Pulmonology, Rochester, NY, United States; Department of Pediatrics, Division of Neonatology, Rochester, NY, United States; Department of Pediatrics, Program in Pediatric Molecular and Personalized Medicine, University of Rochester Medical Center, Rochester, NY, United States. , (United States)
Type
Published Article
Journal
Toxicology letters
Publication Date
Jun 01, 2020
Volume
325
Pages
25–33
Identifiers
DOI: 10.1016/j.toxlet.2020.02.012
PMID: 32112875
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Diacetyl (DA; 2,3-butanedione) is a chemical found commonly in foods and e-cigarettes. When inhaled, DA causes epithelial injury, though the mechanism of repair remain poorly understood. The objective of this study was to evaluate airway basal cell repair after DA vapor exposure. Primary human bronchial epithelial cells were exposed to DA or PBS for 1 h. Lactate dehydrogenase, cleaved caspase 3/7 and trans-epithelial electrical resistance were measured prior to and following exposure. Exposed cultures were analyzed for the airway basal cell markers keratin 5 and p63 as well as ubiquitin and proteasome activity. Cultures were also treated with a proteasome inhibitor (MG132). DA vapor exposure caused a transient decrease in trans-epithelial electrical resistance in all DA-exposed cultures. Supernatant lactate dehydrogenase and cleaved caspase 3/7 increased significantly at the highest DA concentration but not at lower DA concentrations. Increased keratin 5 ubiquitination occurred after DA exposure but resolved by day 3. Damage to airway basal cells persisted at day 3 in the presence of MG132. Diacetyl exposure results in airway basal cell injury with keratin 5 ubiquitination and decreased p63 expression. The ubiquitin-proteasome-pathway partially mediates airway basal cell repair after acute DA exposure. Copyright © 2020 Elsevier B.V. All rights reserved.

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