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Protease activated receptor-2 expression and function in asthmatic bronchial smooth muscle
Benoit Allard1, Imane Bara1, Guillaume Gilbert1
1Univ- Bordeaux, Centre de Recherche Cardio-Thoracique de Bordeaux, U1045, Département de Pharmacologie, Bordeaux, France ; INSERM, Centre de Recherche Cardio-Thoracique de Bordeaux, U1045, Bordeaux, France.
Plos One
|February 20, 2014
Summary
Asthmatic bronchial smooth muscle cells show higher levels of protease-activated receptor-2 (PAR-2), leading to increased calcium responses. Prolonged PAR-2 stimulation promotes proliferation in asthmatic cells, linked to ERK phosphorylation.
Area of Science:
- Cell Biology
- Respiratory Medicine
- Immunology
Background:
- Asthma involves bronchial smooth muscle (BSM) remodeling and mast cell degranulation.
- Mast cell tryptase activates protease-activated receptor type-2 (PAR-2) on BSM cells.
Purpose of the Study:
- Evaluate PAR-2 expression in asthmatic vs. non-asthmatic BSM cells.
- Analyze the impact of prolonged PAR-2 stimulation on asthmatic BSM cell signaling and proliferation.
Main Methods:
- Assessed PAR-2 expression (mRNA, protein) via flow cytometry, western blot, and RT-PCR.
- Measured calcium response, signaling pathways (ERK phosphorylation), and proliferation after PAR-2 stimulation (SLIGKV-NH2, trypsin).
- Utilized lentivirus to modulate PAR-2 expression in control BSM cells.
Main Results:
- Asthmatic BSM cells exhibited higher basal PAR-2 mRNA, protein, and calcium response.
- PAR-2 over-expression in control cells mimicked asthmatic calcium responses.
- Repeated PAR-2 stimulation increased asthmatic BSM cell proliferation, associated with elevated ERK phosphorylation, unlike control cells.
Conclusions:
- Asthmatic BSM cells possess elevated baseline functional PAR-2, contributing to increased calcium signaling.
- Enhanced proliferation in asthmatic BSM cells under prolonged PAR-2 stimulation is mediated by increased ERK phosphorylation.
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