Endothelin-1 directs airway remodeling and hyper-reactivity in a murine asthma model.

ABSTRACT:

Background

The current paradigm describing asthma pathogenesis recognizes the central role of abnormal epithelial function in the generation and maintenance of the disease. However, the mechanisms responsible for the initiation of airway remodeling, which contributes to decreased lung function, remain elusive. Therefore, we aimed to determine the role of altered pulmonary gene expression in disease inception and identify proremodeling mediators.

Methods

Using an adenoviral vector, we generated mice overexpressing smad2, a TGF-β and activin A signaling molecule, in the lung. Animals were exposed to intranasal ovalbumin (OVA) without systemic sensitization.

Results

Control mice exposed to inhaled OVA showed no evidence of pulmonary inflammation, indices of remodeling, o

SUBMITTER: Gregory LG 

PROVIDER: S-EPMC3992903 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature