Abstract
Controlling the inflammatory response to restore tissue homeostasis is a crucial step to maintain tooth vitality after pathogen removal from caries-affected dental tissues. The nuclear peroxisome proliferator-activated receptor beta/delta (PPARβ/δ) is a ligand-activated transcription factor with emerging anti-inflammatory roles in many cells and tissues. However, its expression and functions are poorly understood in human dental pulp cells (hDPCs). Thus, this study evaluated PPARβ/δ expression and assessed the anti-inflammatory effects evoked by activation of PPARβ/δ in lipopolysaccharide- (LPS-) induced hDPCs. Our results showed that hDPCs constitutively expressed PPARβ/δ mRNA/protein, and treatment with LPS increased PPARβ/δ mRNA expression. The selective PPARβ/δ agonist GW0742 significantly decreased inflammation-related mRNA expression in hDPCs (IL6, IL1β, TNFα, MMP1, and MMP2) and RAW264.7 cells (Il6 and Tnfα). Further, PPARβ/δ agonist attenuated MMP2/9 gelatinolytic activity in hDPCs. Previously LPS-conditioned hDPCs increased the migration of RAW264.7 cells through the membrane of a Transwell coculture system. Conversely, pretreatment with GW0742 markedly decreased macrophage recruitment. These findings provide among the first evidence that hDPCs express PPARβ/δ. In addition, they suggest that activation of PPARβ/δ by GW0742 can attenuate some cellular and molecular in vitro aspects related to the inflammatory process, pointing out to investigate its potential target role in dental pulp inflammation.
Highlights
After traumatic injuries and dental caries, a natural defense response takes place within the dentin-pulp complex
We provide among the first evidence of PPARβ/δ mRNA and protein expression in dental pulp cells
We revealed that PPARβ/δ activation by the specific ligand GW0742 improved the inflammatory profile by attenuating some aspects related with the inflammatory process, including proinflammatory cytokine gene expression, MMP gene expression, gelatinase activity, and macrophage recruitment
Summary
After traumatic injuries and dental caries, a natural defense response takes place within the dentin-pulp complex. When controlled and self-limited, resolving inflammation stimulates regenerative events [1] These culminate in reactionary dentin production by the primary odontoblasts [2] or, if these cells die, in reparative dentin production by the stem/progenitor cells present in the pulp tissue [3]. While relatively low levels of cytokines and growth factors can stimulate repair, high amounts of these molecules, as a result of more intense/persistent bacterial challenges and inflammation, can actively inhibit tertiary dentinogenesis [9].
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