ArticleThe international journal of biochemistry & cell biology2008
Protease-activated receptor-2 (PAR-2) is a weak enhancer of mucin secretion by human bronchial epithelial cells in vitro.
Article in The international journal of biochemistry & cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Protease-activated receptor-2 (PAR2) mutation attenuates airway fibrosis in mice during the exacerbation of house dust mite‑induced allergic lung disease by multi‑walled carbon nanotubes.Respiratory research · 2025Article
- Integrated OMICs Approach for the Group 1 Protease Mite-Allergen of House Dust MiteInternational journal of molecular sciences · 2022Article
- PAR-2-activated secretion by airway gland serous cells: role for CFTR and inhibition byAmerican journal of physiology. Lung cellular and molecular physiology · 2021Article
- Investigating the role of MRGPRC11 and capsaicin-sensitive afferent nerves in the anti-influenza effects exerted by SLIGRL-amide in murine airways.Respiratory research · 2016Article
- Membrane-anchored Serine Protease Matriptase Is a Trigger of Pulmonary Fibrogenesis.American journal of respiratory and critical care medicine · 2016Article
- Increased production of BDNF in colonic epithelial cells induced by fecal supernatants from diarrheic IBS patients.Scientific reports · 2015Article
- A highly potent agonist to protease-activated receptor-2 reveals apical activation of the airway epithelium resulting in Ca2+-regulated ion conductance.American journal of physiology. Cell physiology · 2014Article
- Allergic sensitization enhances anion current responsiveness of murine trachea to PAR-2 activation.Pflugers Archiv : European journal of physiology · 2012Article
- Protease-activated receptor 2 mediates mucus secretion in the airway submucosal gland.PloS one · 2012Article
- Receptor-promoted exocytosis of airway epithelial mucin granules containing a spectrum of adenine nucleotides.The Journal of physiology · 2010Article
- German cockroach frass proteases modulate the innate immune response via activation of protease-activated receptor-2.Journal of innate immunity · 2010Article
- Over-expression and localization of a host protein on the membrane of Cryptosporidium parvum infected epithelial cells.Molecular and biochemical parasitology · 2009Article
- Article
- A severe deficiency of coagulation factor VIIa results in attenuation of the asthmatic response in mice.American journal of physiology. Lung cellular and molecular physiology · 2009Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
PAR-2, a member of a family of G-protein-coupled receptors, can be activated by serine proteases via proteolytic cleavage. PAR-2 expression is known to be upregulated in respiratory epithelium subsequent to inflammation in asthma and chronic obstructive pulmonary disease (COPD). Since these diseases also are characterized by excessive mucus production and secretion, we investigated whether PAR-2 could be linked to mucin hypersecretion by airway epithelium. Normal human bronchial epithelial (NHBE) cells in primary culture or the human bronchial epithelial cell lines, NCI-H292 and HBE-1, were used. NHBE, NCI-H292, and HBE-1 cells expressed prominent levels of PAR-2 protein. Short-term (30min) exposure of cells to the synthetic PAR-2 agonist peptide (SLIGKV-NH2) elicited a small but statistically significant increase in mucin secretion at high concentrations (100microM and 1000microM), compared to a control peptide with reversed amino acid sequence (VKGILS-NH2). Neither human lung tryptase nor bovine pancreatic trypsin, both PAR-2 agonists, affected NHBE cell mucin secretion when added over a range of concentrations. Knockdown of PAR-2 expression by siRNA blocked the stimulatory effect of the AP. The results suggest that, since PAR-2 activation only weakly increases mucin secretion by human airway epithelial cells in vitro, PAR-2 probably is not a significant contributor to mucin hypersecretion in inflamed airways.
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