JNK Activation is Responsible for Mucus Overproduction in Smoke Inhalation Injury

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JNK Activation is Responsible for Mucus Overproduction in Smoke Inhalation Injury

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dc.contributor.author Choi, Won-II
dc.contributor.author Kwon, Kun Young
dc.contributor.author Quinn, Deborah A
dc.contributor.author Syrkina, Olga L.
dc.contributor.author Hales, Charles Albert
dc.date.accessioned 2012-02-24T00:33:16Z
dc.date.issued 2010
dc.identifier.citation Choi, Won-II, Olga Syrkina, Kun Young Kwon, Deborah A. Quinn, and Charles A. Hales. 2010. JNK activation is responsible for mucus overproduction in smoke inhalation injury. Respiratory Research 11(1): 172. en_US
dc.identifier.issn 1465-9921 en_US
dc.identifier.uri http://nrs.harvard.edu/urn-3:HUL.InstRepos:8231696
dc.description.abstract Background: Increased mucus secretion is one of the important characteristics of the response to smoke inhalation injuries. We hypothesized that gel-forming mucins may contribute to the increased mucus production in a smoke inhalation injury. We investigated the role of c-Jun N-terminal kinase (JNK) in modulating smoke-induced mucus secretion. Methods: We intubated mice and exposed them to smoke from burning cotton for 15 min. Their lungs were then isolated 4 and 24 h after inhalation injury. Three groups of mice were subjected to the smoke inhalation injury: (1) wild-type (WT) mice, (2) mice lacking JNK1 (JNK1-/- mice), and (3) WT mice administered a JNK inhibitor. The JNK inhibitor (SP-600125) was injected into the mice 1 h after injury. Results: Smoke exposure caused an increase in the production of mucus in the airway epithelium of the mice along with an increase in MUC5AC gene and protein expression, while the expression of MUC5B was not increased compared with control. We found increased MUC5AC protein expression in the airway epithelium of the WT mice groups both 4 and 24 h after smoke inhalation injury. However, overproduction of mucus and increased MUC5AC protein expression induced by smoke inhalation was suppressed in the JNK inhibitor-treated mice and the JNK1 knockout mice. Smoke exposure did not alter the expression of MUC1 and MUC4 proteins in all 3 groups compared with control. Conclusion: An increase in epithelial MUC5AC protein expression is associated with the overproduction of mucus in smoke inhalation injury, and that its expression is related on JNK1 signaling. en_US
dc.language.iso en_US en_US
dc.publisher BioMed Central en_US
dc.relation.isversionof doi:10.1186/1465-9921-11-172 en_US
dc.relation.hasversion http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014901/pdf/ en_US
dash.license LAA
dc.title JNK Activation is Responsible for Mucus Overproduction in Smoke Inhalation Injury en_US
dc.type Journal Article en_US
dc.description.version Version of Record en_US
dc.relation.journal Respiratory Research en_US
dash.depositing.author Hales, Charles Albert
dc.date.available 2012-02-24T00:33:16Z
dash.affiliation.other HMS^Medicine-Massachusetts General Hospital en_US

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