PPAR激动剂
过氧化物酶体增殖物激活受体
炎症
脂多糖
细胞生物学
过氧化物酶体增殖物激活受体δ
兴奋剂
受体
牙髓干细胞
肿瘤坏死因子α
化学
体外
牙髓(牙)
免疫学
生物
转录因子
核受体
医学
生物化学
牙科
基因
作者
Caroline Lourenço de Lima,Bruna Rabelo Amorim,Carine Royer,Augusto Pereira Resende,Maria de Fátima Borin,Francisco de Assis Rocha Neves,Ana Carolina Acevedo
出处
期刊:Ppar Research
[Hindawi Limited]
日期:2021-03-18
卷期号:2021: 1-10
被引量:1
摘要
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.
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