The aim of this study was to use immunohistochemistry and an ex vivo murine airway myograph assay to confirm the presence in murine lung of PAR2 as a functional airway modulator.
PAR2 (detected using Alomone APR-32 antibody) was present on both murine airway and lung tissue. Following exposure to a disease relevant challenge (oxidative stress), PAR2 activation with trypsin (10 U ml-1), was observed to induce a higher relaxation in airway segments pre-contracted with acetylcholine (1 µM) using wire myography. Specifically, tracheal segments subjected to oxidative stress showed a significantly higher percentage relaxation (mean ± SEM; 53.8%±10.3%) compared with control (30.8%±7.9%; p=0.05; n=4). A higher percentage relaxation was also observed in bronchial segments (oxidative 55.1%±10.7% vs. control 33.9%±1.2%; p=0.07; n=4). The trypsin-induced relaxation was confirmed to be PAR2-dependent since relaxation to trypsin was significantly reduced in tracheal and bronchial tissue derived from PAR2-knockout mice.
Taken together this data confirms that PAR2 is present and suggests the receptor contributes functionally to the modulation of ASM tone in mice.
|Publication status||Published - 10 Sept 2019|
|Event||British Association for Lung Research Summer Meeting 2019: Lung Injury and Repair - Cambridge University, Selwyn College, Cambridge , United Kingdom|
Duration: 10 Sept 2019 → 12 Sept 2019
|Conference||British Association for Lung Research Summer Meeting 2019|
|Period||10/09/19 → 12/09/19|