Cigarette Smoke Impairs A2A Adenosine Receptor Mediated Wound Repair through Up-regulation of Duox-1 Expression View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Zhi Tian, Hui Zhang, Jendayi Dixon, Nicole Traphagen, Todd A Wyatt, Kusum Kharbanda, Samantha Simet Chadwick, Narasaiah Kolliputi, Diane S Allen-Gipson

ABSTRACT

Cigarette smoke (CS) exposure and intrinsic factors such as the NADPH oxidases produce high levels of reactive oxygen species (ROS), ensuing inflammatory tissue injury. We previously demonstrated that CS-generated ROS, particularly hydrogen peroxide (H2O2), impaired adenosine stimulated wound repair. We hypothesized that CS exposure modulates expression of Dual oxidase 1 (Duox-1), a NADPH oxidases known to generate H2O2. To test this hypothesis, we used human bronchial epithelial cell line Nuli-1 and C57BL/6 mice. Cells were treated with 5% CS extract (CSE) for various periods of time, and mice were exposed to whole body CS for six weeks. Both CSE and CS treatment induced increased expression of Duox-1, and silencing of Doux-1 improved the rate of cell wound repair induced by CSE treatment. Nuli-1 cells pretreated with thapsigargin but not calcium ionophore exhibited increased Duox-1 mRNA expression. CSE treatment stimulated PKCα activation, which was effectively blocked by pretreatment with diphenylene iodonium, a NADPH oxidase inhibitor. Compared to control, lungs from CS-exposed mice showed a significant increase in PKCα activity and Duox-1 expression. Collectively, the data demonstrated that CS exposure upregulates expression of Duox-1 protein. This further leads to H2O2 production and PKCα activation, inhibiting A2AAR-stimulated wound repair. More... »

PAGES

44405

References to SciGraph publications

  • 2013-11. Genome engineering using the CRISPR-Cas9 system in NATURE PROTOCOLS
  • 2008-07. NOX enzymes as novel targets for drug development in SEMINARS IN IMMUNOPATHOLOGY
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    http://scigraph.springernature.com/pub.10.1038/srep44405

    DOI

    http://dx.doi.org/10.1038/srep44405

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1084132295

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28337995


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