Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 359, Issue 3, Pages 691-696Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2007.05.170
Keywords
PAK2; PAK4; MUC5AC; NTHi; EGF; p38; ERK
Categories
Funding
- NHLBI NIH HHS [P01 HL077789, HL077789] Funding Source: Medline
- NIDCD NIH HHS [R01 DC005843-05, DC004562, R01 DC005843-03, R01 DC004562-07, R01 DC005843-04, R01 DC005843-01, R01 DC005843, R01 DC004562-06, R01 DC005843-02, R01 DC005843-06, R01 DC004562-09, R01 DC004562-08, DC005843, R01 DC004562] Funding Source: Medline
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Mucin, a major component of mucus, plays a critical role in host mucosal defense response by participating in mucociliary clearance. However, if overproduced, overproduced mucus leads to airway mucus obstruction and conductive hearing loss. Despite extensive studies that focus on investigating how MUC5AC mucin is regulated by one inducer at a time, how MUC5AC is synergistically regulated by multiple factors remains unknown. Here we provide direct evidence for the first time that bacterial pathogen NTHi and human growth factor EGF synergize with each other to potently up-regulate MUC5AC mucin transcription. Moreover, activation of both p38 and ERK is required for synergistic induction of MUC5AC by NTHi and EGF. Finally, PAK2 and PAK4 are differentially involved in this synergistic induction of MUC5AC by acting upstream of p38 and ERK. Our studies bring novel insights into our understanding of synergistic regulation of MUC5AC mucin by both pathological and physiological inducers. (c) 2007 Elsevier Inc. All rights reserved.
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