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Kyoung Seob Song 2 Articles
STAT3 inhibition decreases ATP-induced MUC8 gene expression in human airway epithelial cells
Cheol Hong Kim, Kyoung Seob Song
Kosin Med J. 2022;37(2):134-139.   Published online June 24, 2022
DOI: https://doi.org/10.7180/kmj.22.102
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Abstract PDFPubReader   ePub   CrossRef-TDMCrossref - TDM
Background
Contact between the human pulmonary system and bacteria, viruses, or other pathogens can induce airway diseases. Although pathogen-induced mucus oversecretion and hyperproduction are frequently observed in the human respiratory tract, the molecular mechanisms of pathogen-induced mucus hypersecretion and overproduction remain unclear. The objective of this study was to investigate the physiological signaling mechanism of ATP-induced MUC8 gene expression in human airway epithelial cells.
Methods
Real-time reverse transcription polymerase chain reaction, a cytokine array, and a Ca2+ concentration assay were performed to investigate the ATP/P2Y2-induced MUC8 gene expression levels in human airway epithelial cells.
Results
The ATP/P2Y2 complex robustly secreted interleukin (IL)-6 in a time-dependent manner, whereas siRNA-P2Y2 did not. Moreover, ATP/P2Y2 induced MUC8 gene expression. IL-6 secreted by ATP strongly elevated ATP/P2Y2-induced MUC8 gene expression compared to ATP/P2Y2. Interestingly, a specific STAT3 inhibitor, 5,15-DPP, dramatically inhibited ATP/P2Y2/IL-6-induced STAT3 phosphorylation and resulted in an approximately 5-fold decrease in MUC8 gene expression.
Conclusions
We showed that IL-6-activated STAT6 is essential for ATP/P2Y2-induced MUC8 gene expression as part of inflammatory signaling by cytokines during airway inflammation. Our results provide a new molecular understanding of the signaling mechanism of MUC8 gene expression during airway inflammation.
Regulatory Mechanism of Mucous Hyperproduction in the Airway
Kyoung Seob Song
Kosin Med J. 2010;25(2):1-5.   Published online December 31, 2010
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KMJ : Kosin Medical Journal