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Regulation of a novel airway glandular mucin by smoke

Institution: University of California, Davis
Investigator(s): Yin Chen, Ph.D.
Award Cycle: 2004 (Cycle 13) Grant #: 13KT-0101 Award: $126,126
Subject Area: Pulmonary Disease
Award Type: New Investigator Awards

Initial Award Abstract
This study is to understand the cause of mucus overproduction (generating excessive mucus) at the molecular level. Mucus overproduction has been observed in many airway diseases including COPD. Excessive mucus causes airway obstruction that increases the morbidity and mortality of COPD. The major macromolecular components of the mucus are high-molecular-weight mucin glycoproteins. Mucins determine the viscoelastic property (stickiness) of mucus and play an important role in the development of airway obstruction. Two major sources generate airway mucin: surface epithelial cells and submucosal gland. Many studies are focused on the surface cells, while few works have been carried out on the gland cells. In this study, we focus on a novel mucin gene-MUC19 that is submucosal gland specific and highly elevated by smoke. We plan 1) to determine whether MUC19 protein is elevated in the airway secretion of COPD and non-COPD smoker; 2) to identify the transcriptional factor triggered by smoke that drives MUC19 expression; 3) to identify the signaling pathway triggered by smoke that transduces the signal into the cells to cause the increased expression of MCU19. Successful completion of this project will not only further our understanding of the pathogenesis of COPD but also help to identify useful molecular targets for the development of efficient therapeutic methods.