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ABSTRACT: Background
Airway smooth muscle cells (ASMC) play a key role in bronchial hyperresponsiveness (BHR). A major component of the signaling cascade leading to ASMC contraction is calcium. So far, agonist-induced Ca2+-signaling in asthma has been studied by comparing innate properties of inbred rat or mouse strains, or by using selected mediators known to be involved in asthma. T-bet knock-out (KO) mice show key features of allergic asthma such as a shift towards TH2-lymphocytes and display a broad spectrum of asthma-like histological and functional characteristics. In this study, we aimed at investigating whether Ca2+-homeostasis of ASMC is altered in T-bet KO-mice as an experimental model of asthma.Methods
Lung slices of 100 to 200 microm thickness were obtained from T-bet KO-
SUBMITTER: Bergner A
PROVIDER: S-EPMC1395308 | biostudies-literature | 2006 Feb
REPOSITORIES: biostudies-literature