MAP 激酶通路通过 p38 磷酸化参与成牙本质细胞的刺激。
The MAP kinase pathway is involved in odontoblast stimulation via p38 phosphorylation.
机构信息
Laboratoire de Physiopathologie Orale Moléculaire, INSERM, Centre de Recherche des Cordeliers, Paris, France.
出版信息
J Endod. 2010 Feb;36(2):256-9. doi: 10.1016/j.joen.2009.09.019. Epub 2009 Dec 10.
INTRODUCTION
We have previously shown that the p38 gene is highly expressed in odontoblasts during active primary dentinogenesis, but is drastically down-regulated as cells become quiescent in secondary dentinogenesis. Based on these observations, we hypothesized that p38 expression might be upregulated, and the protein activated by phosphorylation, when odontoblasts are stimulated such as during tertiary reactionary dentinogenesis.
METHODS
We stimulated immortalized, odontoblast-like MDPC-23 cells, alone or in combination, with heat-inactivated Streptococcus mutans, EDTA-extracted dentine matrix proteins (DMPs), or growth factors, including transforming growth factor (TGF)-beta1, tumor necrosis factor-alpha (TNF-alpha), and adrenomedullin (ADM). We used ELISA to measure the resulting phosphorylation of the p38 protein, as well as its degree of nuclear translocation.
RESULTS
Our results suggest that the p38-MAPKinase pathway is activated during odontoblast stimulation in tertiary dentinogenesis by both p38 phosphorylation and enhanced nuclear translocation.
CONCLUSIONS
Data indicate that odontoblast behaviour therefore potentially recapitulates that during active primary dentinogenesis.
简介
我们之前已经表明，p38 基因在原发性牙本质形成过程中的成牙本质细胞中高度表达，但在继发性牙本质形成过程中成牙本质细胞静止时其表达会急剧下调。基于这些观察，我们假设当成牙本质细胞受到刺激时，如在第三反应性牙本质形成过程中，p38 的表达可能会被上调，并且其蛋白通过磷酸化而被激活。
方法
我们单独或联合使用热失活变形链球菌、EDTA 提取的牙本质基质蛋白（DMPs）或生长因子（包括转化生长因子（TGF）-β1、肿瘤坏死因子-α（TNF-α）和肾上腺髓质素（ADM））刺激永生化的成牙本质细胞样 MDPC-23 细胞。我们使用 ELISA 来测量 p38 蛋白的磷酸化程度及其核转位程度。
结果
我们的结果表明，p38-MAPK 途径在第三反应性牙本质形成过程中成牙本质细胞的刺激中被激活，表现为 p38 磷酸化和增强的核转位。
结论
数据表明，成牙本质细胞的行为因此可能再现了活跃的原发性牙本质形成过程中的情况。
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