Nicotine Affects Multiple Biological Processes in EpiDermTM Organotypic Tissues and Keratinocyte Monolayers

Nicotine Affects Multiple Biological Processes in EpiDermTM Organotypic Tissues and Keratinocyte Monolayers

Dermal exposure to nicotine is common due to the widespread use of tobacco products. Here, we assessed the effects of nicotine at concentrations found in thirdhand smoke (THS) contaminated environments and electronic cigarette (EC) spills or leaks on a 3D human skin model (EpiDermTM) and on submerge...

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Bibliographic Details
Published in:Atmosphere Vol. 13; no. 5; p. 810
Main Authors: Pozuelos, Giovanna L., Rubin, Matine, Vargas, Samantha, Ramirez, Erik, Bandaru, Dhiresh, Sha, Jihui, Wohlschlegel, James, Talbot, Prue
Format: Journal Article
Language:English
Published: Basel MDPI AG 16-05-2022
Subjects:
Apoptosis
Biological activity
Cell adhesion
Cells
Chemical spills
Damage
dermal exposure
electronic cigarettes
EpiDermTM
Exposure
Homeostasis
Keratinocytes
Mitochondria
Monomolecular films
Morphology
Nicotine
Organelles
Peptides
Peroxisomes
Phenotypes
Plasmids
Protein biosynthesis
Protein synthesis
Proteins
Proteomes
Proteomics
Skin
Smoking
Spills
thirdhand smoke
Three dimensional models
Tobacco
Transdermal medication
Vaping
Western blotting
Wound healing
United States > US
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Summary:Dermal exposure to nicotine is common due to the widespread use of tobacco products. Here, we assessed the effects of nicotine at concentrations found in thirdhand smoke (THS) contaminated environments and electronic cigarette (EC) spills or leaks on a 3D human skin model (EpiDermTM) and on submerged keratinocyte cultures. Air liquid interface treatment of EpiDermTM with 10 or 400 μg/mL of nicotine for 24 h followed by proteomics analysis showed altered pathways related to inflammation, protein synthesis, cell–cell adhesion, apoptosis, and mitochondrial function. Submerged cultured keratinocytes were used to validate the proteomics data and further characterize the response of skin cells to nicotine. Mitochondrial phenotype changed from networked to punctate in keratinocytes treated with 10 or 400 μg/mL of nicotine for 48 h and 24 h, respectively. After 72 h, all concentrations of nicotine caused a significant decrease in the networked phenotype. In Western blots, keratinocytes exposed to 400 μg/mL of nicotine had a significant decrease in mitofusin 2, while mitofusin 1 decreased after 72 h. The shift from networked to punctate mitochondria correlated with a decrease in mitofusin 1/2, a protein needed to establish and maintain the networked phenotype. Mitochondrial changes were reversible after a 24 h recovery period. Peroxisomes exposed to 400 μg/mL of nicotine for 24 h became enlarged and were fewer in number. Nicotine concentrations in THS and EC spills altered the proteome profile in EpiDermTM and damaged organelles including mitochondria and peroxisomes, which are involved in ROS homeostasis. These changes may exacerbate skin infections, inhibit wound healing, and cause oxidative damage to cells in the skin.
ISSN:2073-4433
2073-4433
DOI:10.3390/atmos13050810