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PAR-2 regulates dental pulp inflammation associated with caries
F T Lundy1, I About, T M Curtis
1Centre for Infection and Immunity, School of Medicine, Dentistry and Biomedical Sciences, Whitla Medical Building, Queen's University Belfast, 97 Lisburn Road, Belfast BT9 7BL, United Kingdom. f.lundy@qub.ac.uk
Journal of Dental Research
|May 28, 2010
Summary
Protease-activated receptor-2 (PAR-2) is upregulated in dental caries, indicating its role in pulpal inflammation. Activated PAR-2 increases cyclo-oxygenase-2 (COX-2) expression, a key inflammatory mediator.
Area of Science:
- Immunology
- Oral Biology
- G-protein coupled receptor signaling
Background:
- Protease-activated receptors (PARs) are G-protein coupled receptors activated by protease cleavage.
- PARs play a role in inflammatory responses.
- The role of PAR-2 in dental caries and pulpal inflammation is not well understood.
Purpose of the Study:
- To investigate the expression and activation of PAR-2 in dental caries.
- To determine if PAR-2 activation influences pro-inflammatory mediator expression in dental pulp.
Main Methods:
- Immunohistochemistry was used to assess PAR-2 localization in human dental pulp tissue.
- In vitro functional assays were performed using pulp cells stimulated with trypsin, a PAR-2 agonist (PAR2-AP), and endogenous molecules from carious and healthy teeth.
- Cyclo-oxygenase-2 (COX-2) expression was measured following PAR-2 activation.
Main Results:
- PAR-2 was significantly expressed in pulp cells subjacent to caries lesions but minimally in healthy pulp.
- Pulp cell lysates from carious teeth, but not healthy teeth, contained endogenous molecules that activated PAR-2.
- In vitro activation of PAR-2 increased the expression of the pro-inflammatory mediator COX-2.
Conclusions:
- PAR-2 is expressed and activated in dental caries.
- PAR-2 activation in dental pulp cells leads to increased COX-2 expression, suggesting a role in pulpal inflammation.
- PAR-2 represents a potential therapeutic target for managing dental caries-associated inflammation.
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