Journal
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
Volume 40, Issue 2, Pages 168-178Publisher
AMER THORACIC SOC
DOI: 10.1165/rcmb.2007-0377OC
Keywords
MUC5B; estrogen; ER alpha; CREB
Funding
- Korea Research Foundation [KRF-2005-015-E00163]
- Korea Science and Engineering Foundation
- Korea government (MOST) [R11-2007-040-02001-0]
- National Research Foundation of Korea [R11-2007-040-02001-0, 2005-015-E00163, 2007-0056416] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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MUC5B is a major mucin of the human respiratory tract, and it is not clear how MUC5B expression is regulated in various airway diseases. The goal of this study was to determine the mechanisms by which 17 beta-estradiol induces MUC5B gene expression in airway epithelial cells. It was found that E2, a sex hormone, stimulates MUC5B gene overexpression by interaction with estrogen receptor alpha (ER alpha) and by acting through extracellular signal-regulated kinase 1/2 (ERK1/2)mitogen-activated protein kinase (MAPK). Pretreatment with ER antagonist ICl 182,780 blocked both E2-induced ERK1/2-MAPK activation and MUC5B gene expression. It was also found that the activation of p90 ribosomal S 6 protein kinase 1 (RSK1), cAMP-response element-binding protein (CREB), and cAMP-response element (CRE) (-956 region of the MUC5B promoter)-responsive signaling cascades via ERK1/2 MAPK are crucial aspects of the intracellular mechanisms that mediate MUC5B gene expression. Taken together, these studies give additional insights into the molecular mechanism of hormone-induced MUC5B gene expression and enhance our understanding of abnormal mucin secretion in response to hormonal imbalances.
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