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Related Experiment Videos

Malondialdehyde-acetaldehyde adducts decrease bronchial epithelial wound repair.

Todd A Wyatt1, Kusum K Kharbanda, Dean J Tuma

  • 1Research Service, Department of Veterans Affairs Medical Center, 4101 Woolworth Avenue, Omaha, NE 68105, USA. twyatt@unmc.edu

Alcohol (Fayetteville, N.Y.)
|November 1, 2005
PubMed
Summary
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Alcohol and cigarette smoke exposure can impair bronchial epithelial cell wound repair. Malondialdehyde-acetaldehyde adducts activate protein kinase C (PKC) via scavenger receptors, hindering healing.

Area of Science:

  • Cell biology
  • Toxicology
  • Pulmonary medicine

Background:

  • Alcohol abuse and cigarette smoking are common comorbidities.
  • Malondialdehyde and acetaldehyde adducts activate protein kinase C (PKC) in bronchial cells.
  • PKC plays a role in regulating bronchial epithelial cell wound repair.

Purpose of the Study:

  • To investigate if malondialdehyde-acetaldehyde adducts decrease bronchial epithelial cell wound repair through scavenger receptors.
  • To determine the role of protein kinase C (PKC) alpha in this process.

Main Methods:

  • Confluent bovine bronchial epithelial cell monolayers were wounded in serum-free media.
  • Cells were treated with bovine serum albumin adducted with malondialdehyde and acetaldehyde (BSA-MAA) or fucoidan.

Related Experiment Videos

  • Protein kinase C (PKC) alpha inhibitor (Gö 6976) and Western blot were used to analyze scavenger receptor presence and pathway activation.

    • Main Results:

    • BSA-MAA inhibited bronchial epithelial cell wound closure in a dose-dependent manner (up to 60%).
    • Fucoidan, a scavenger receptor ligand, also inhibited wound repair and blocked BSA-MAA binding.
    • PKC alpha inhibition prevented BSA-MAA and fucoidan-induced inhibition of wound closure.
    • Scavenger receptors (SRA, SRBI, SRBII, CD36) were detected on bronchial epithelial cell membranes.

    Conclusions:

    • Scavenger receptor-mediated activation of PKC alpha reduces bronchial epithelial cell wound healing.
    • This mechanism may be relevant in conditions involving alcohol and cigarette smoke exposure.
    • Malondialdehyde-acetaldehyde adducts contribute to impaired lung tissue repair.