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

PPAR Research ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Caroline L. de Lima ◽  
Bruna R. Amorim ◽  
Carine Royer ◽  
Augusto P. Resende ◽  
Maria F. Borin ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Dental Pulp ◽  
Raw264.7 Cells ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Pulp Inflammation ◽  
Human Dental Pulp ◽  
Pulp Cells ◽  
Anti Inflammatory

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.

In vitro culture of human dental pulp cells: some aspects of cells emerging early from the explant

1997 ◽  
Vol 1 (3) ◽  
pp. 131-140 ◽  
Author(s):  
L. Stanislawski ◽  
J. P. Carreau ◽  
M. Pouchelet ◽  
Z. H. J. Chen ◽  
M. Goldberg
Keyword(s):  
In Vitro Culture ◽  
Dental Pulp ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Human Dental Pulp ◽  
Pulp Cells

scholarly journals Highly Proliferative Immortalized Human Dental Pulp Cells Retain the Odontogenic Phenotype when Combined with a Beta-Tricalcium Phosphate Scaffold and BMP2

2020 ◽  
Vol 2020 ◽  
pp. 1-18 ◽  
Author(s):  
Xiangfen Li ◽  
Liu Wang ◽  
Qin Su ◽  
Ling Ye ◽  
Xuedong Zhou ◽  
...  
Keyword(s):  
Tricalcium Phosphate ◽  
Dental Pulp ◽  
Biological Behavior ◽  
Dental Pulp Cells ◽  
Differentiation Potential ◽  
Human Dental Pulp Cells ◽  
Beta Tricalcium Phosphate ◽  
Human Dental Pulp ◽  
Pulp Cells

Human dental pulp cells (HDPCs) play a vital role in dentin formation and reparative dentinogenesis, which indicated their potential application in regenerative medicine. However, HDPCs, which can only be obtained from scarce human pulp tissues, also have a limited lifespan in vitro, and stem cells usually lose their original characteristics over a large number of passages. To overcome these challenges, we successfully immortalized human dental pulp cells using the piggyBac system which was employed to efficiently overexpress the SV40 T-Ag, and we then comprehensively described the cell biological behavior. The immortalized human dental pulp cells (iHDPCs) acquired long-term proliferative activity and expressed most HDPC markers. The iHDPCs maintained multiple differentiation potential and could be induced to differentiate into chondrogenic, osteogenic, and adipogenic cells in vitro. We also proved that the iHDPCs gained a stronger ability to migrate than the primary cells, while apoptosis was inhibited. Furthermore, highly proliferative iHDPCs displayed no oncogenicity when subcutaneously implanted into athymic nude mice. Finally, iHDPCs exhibited odontogenic differentiation ability and secreted dentin sialophosphoprotein (DSPP) when combined with a beta-tricalcium phosphate scaffold and bone morphogenetic protein-2 (BMP2) in vivo. Conclusively, the established iHDPCs are a valuable resource for mechanistic study of dental pulp cell differentiation and dental pulp injury repair, as well as for applications in tooth regeneration.

scholarly journals The Anti-Inflammatory Effect of Human Telomerase-Derived Peptide onP. gingivalisLipopolysaccharide-Induced Inflammatory Cytokine Production and Its Mechanism in Human Dental Pulp Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Yoo-Jin Ko ◽  
Kil-Young Kwon ◽  
Kee-Yeon Kum ◽  
Woo-Cheol Lee ◽  
Seung-Ho Baek ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Map Kinases ◽  
Inhibitory Effect ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Human Dental Pulp ◽  
Pulp Cells ◽  
Anti Inflammatory ◽  
Human Telomerase

Porphyromonas gingivalisis considered with inducing pulpal inflammation and has lipopolysaccharide (LPS) as an inflammatory stimulator. GV1001 peptide has anticancer and anti-inflammation activity due to inhibiting activation of signaling molecules after penetration into the various types of cells. Therefore, this study examined inhibitory effect of GV1001 on dental pulp cells (hDPCs) stimulated byP. gingivalisLPS. The intracellular distribution of GV1001 was analyzed by confocal microscopy. Real-time RT-PCR was performed to determine the expression levels of TNF-αand IL-6 cytokines. The role of signaling by MAP kinases (ERK and p38) was explored using Western blot analysis. The effect of GV1001 peptide on hDPCs viability was measured by MTT assay. GV1001 was predominantly located in hDPC cytoplasm. The peptide inhibitedP. gingivalisLPS-induced TNF-αand IL-6 production in hDPCs without significant cytotoxicity. Furthermore, GV1001 treatment markedly inhibited the phosphorylation of MAP kinases (ERK and p38) in LPS-stimulated hDPCs. GV1001 may preventP. gingivalisLPS-induced inflammation of apical tissue. Also, these findings provide mechanistic insight into how GV1001 peptide causes anti-inflammatory actions in LPS-stimulated pulpitis without significantly affecting cell viability.

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