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KMID : 0624620170500100516
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BMB Reports
2017 Volume.50 No. 10 p.516 ~ p.521
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Airborne particulate matter increases MUC5AC expression by downregulating Claudin-1 expression in human airway cells
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Kim Sang-Su
Kim Cheol-Hong
Kim Ji-Wook
Kung Hsi Chiang
Park Tae-Woo
Shin Yu-Som
Kim Ju-Deok
Ryu Sie-Jeong
Kim Wang-Joon
Choi Yung-Hyun
Song Kyoung-Seob
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Abstract
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CLB2.0, a constituent of PM, induces secretion of multiple cytokines and chemokines that regulate airway inflammation. Specifically, IL-6 upregulates CLB2.0-induced MUC5AC and MUC1 expression. Interestingly, of the tight junction proteins examined, claudin-1 expression was inhibited by CLB2.0. While the overexpression of claudin-1 decreased CLB2.0-induced MUC5AC expression, it increased the expression of the anti-inflammatory mucin, MUC1. CLB2.0-induced IL-6 secretion was mediated by ROS. The ROS scavenger N-acetylcysteine inhibited CLB2.0-induced IL-6 secretion, thereby decreasing the CLB2.0-induced MUC5AC expression, whereas CLB2.0-induced MUC1 expression increased. CLB2.0 activated the ERK1/2 MAPK via a ROS-dependent pathway. ERK1/2 downregulated the claudin-1 and MUC1 expressions, whereas it dramatically increased CLB2.0-induced MUC5AC expression. These findings suggest that CLB2.0-induced ERK1/2 activation acts as a switch for regulating inflammatory conditions though a ROS-dependent pathway. Our data also suggest that secreted IL-6 regulates CLB2.0-induced MUC5AC and MUC1 expression via ROS-mediated downregulation of claudin-1 expression to maintain mucus homeostasis in the airway.
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KEYWORD
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Airway inflammation, Claudin-1, IL-6, MUC1, MUC5AC, PM
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