Journal of endodontics · 2018
Pentraxin 3 Modulates the Inflammatory Response in Human Dental Pulp Cells.
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Kim Yeon, Park Jin-Sung, Park Hyun-Joo, Kim Mi-Kyoung, Kim Yong-Il, Bae Soo-Kyung, Kim Hyung Joon, Jeong Chul-Ho, Bae Moon-Kyoung
Аннотация
INTRODUCTION: Pentraxin 3 (PTX3) has been suggested as a novel inflammatory biomarker in inflammation-associated diseases. The aim of this study was to examine the role of PTX3 in the inflammatory response of human dental pulp cells (HDPCs).
METHODS: HDPCs were treated with tumor necrosis factor alpha (TNF-α), and total RNA and protein were extracted. PTX3 messenger RNA and protein expression levels were analyzed using reverse transcription polymerase chain reaction and Western blotting, respectively. For PTX3 knockdown, HDPCs were transfected with a small interfering RNA against human PTX3. Macrophage chemotaxis after PTX3 silencing in HDPCs was assessed by transwell migration assays.
RESULTS: TNF-α increased PTX3 messenger RNA and protein levels in HDPCs. TNF-α-induced PTX3 expression was mediated by extracellular signal-regulated kinase 1/2 and nuclear factor kappa B. PTX3 knockdown decreased the expression levels of interleukin 6, interleukin 8, and monocyte chemoattractant protein 1 after stimulation with TNF-α in HDPCs. Moreover, PTX3 silencing in HDPCs significantly decreased the chemotactic migration of macrophages.
CONCLUSIONS: Our findings indicate PTX3 plays a critical role in the regulation of pulp inflammatory processes and reveal its underlying molecular mechanism.
METHODS: HDPCs were treated with tumor necrosis factor alpha (TNF-α), and total RNA and protein were extracted. PTX3 messenger RNA and protein expression levels were analyzed using reverse transcription polymerase chain reaction and Western blotting, respectively. For PTX3 knockdown, HDPCs were transfected with a small interfering RNA against human PTX3. Macrophage chemotaxis after PTX3 silencing in HDPCs was assessed by transwell migration assays.
RESULTS: TNF-α increased PTX3 messenger RNA and protein levels in HDPCs. TNF-α-induced PTX3 expression was mediated by extracellular signal-regulated kinase 1/2 and nuclear factor kappa B. PTX3 knockdown decreased the expression levels of interleukin 6, interleukin 8, and monocyte chemoattractant protein 1 after stimulation with TNF-α in HDPCs. Moreover, PTX3 silencing in HDPCs significantly decreased the chemotactic migration of macrophages.
CONCLUSIONS: Our findings indicate PTX3 plays a critical role in the regulation of pulp inflammatory processes and reveal its underlying molecular mechanism.
Предметные рубрики MeSH
C-Reactive ProteinCells, CulturedCytokinesDental PulpGene ExpressionGene Knockdown TechniquesGene SilencingHumansInflammation MediatorsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Molecular Targeted TherapyNF-kappa BPulpitisRNA, MessengerRNA, Small InterferingReverse Transcriptase Polymerase Chain ReactionSerum Amyloid P-ComponentTumor Necrosis Factor-alphaPentraxins