Hyaluronan fragments/CD44 mediate oxidative stress-induced MUC5B up-regulation in airway epithelium.

ABSTRACT: Mucus hypersecretion with elevated MUC5B mucin production is a pathologic feature in many airway diseases associated with oxidative stress. In the present work, we evaluated MUC5B expression in airways and in primary cultures of normal human bronchial epithelial (NHBE) cells, as well as the mechanisms involved in its regulation. We found that oxidative stress generated by cigarette smoke or reactive oxygen species (ROS) induces MUC5B up-regulation in airway epithelium from smokers and in NHBE cells, respectively. We have previously shown that ROS-induced MUC5AC expression in NHBE cells is dependent on hyaluronan depolymerization and epidermal growth factor receptor (EGFR)/mitogen-activated protein kinase (MAPK) activation. Since hyaluronan fragments can activate MAPK through the hyaluronan

SUBMITTER: Casalino-Matsuda SM 

PROVIDER: S-EPMC2645525 | biostudies-literature | 2009 Mar

REPOSITORIES: biostudies-literature