Investigation of PPARβ/δ within Human Dental Pulp Cells: A Preliminary In Vitro Study

Author:

de Lima Caroline L.12ORCID,Amorim Bruna R.1ORCID,Royer Carine2ORCID,Resende Augusto P.1ORCID,Borin Maria F.2ORCID,Neves Francisco A. R.2ORCID,Acevedo Ana Carolina1ORCID

Affiliation:

1. Laboratory of Oral Histopathology, Faculty of Health Sciences, University of Brasilia, University Campus Darcy Ribeiro, Brasília, Brazil

2. Laboratory of Molecular Pharmacology, Faculty of Health Sciences, University of Brasilia, University Campus Darcy Ribeiro, Brasília, Brazil

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.

Funder

Fundação de Apoio à Pesquisa do Distrito Federal

Publisher

Hindawi Limited

Subject

Pharmacology (medical),Drug Discovery

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