Abstract
Introduction Caveolin-1 (Cav-1) and Cavin-2 are fundamental signalling scaffold proteins involved in airway smooth muscle (ASM) contraction; however few is known about their expression in asthma. Objective The expression of Cav-1 and Cavin-2 in an asthma model was evaluated. Methods Antigenic challenges with ovalbumin (OVA) were applied every 10 days to sensitized guinea pigs. Airway obstruction, hyperresponsiveness (AHR), Cavin-2 and Cav-1 expression was evaluated at the third challenge. The control group received saline solution instead of OVA. Results OVA-challenges in sensitized guinea pigs induced airway obstruction, AHR and reduction in lung Cav-1 mRNA (assessed by RT-PCR); nevertheless, flow cytometry in myocytes showed an increment in Cav-1 levels in ASM cells. The immunohistochemistry in lung tissues did not show evident changes in Cav-1 expression in ASM, but revealed a noticeable reduction of Cav-1 in vascular pulmonary smooth muscle (VPSM) in asthma model. The reduction in Cav-1 in VPSM was related to muscle hyperplasia; however, the arterial systemic and pulmonary pressures did not change between asthma model and control guinea pigs. Protein Cavin-2 was also increased in asthma model as seen by Western blot analysis of tracheal smooth muscle. Conclusions Our data suggest that the increment of Cav-1 and Cavin-2 expression in ASM induces a contractile phenotype associated with the development of AHR, while the reduction of Cav-1 in VPSM induces a proliferative phenotype in this asthma model.
- © 2014 ERS
