Ito Mai, Arakawa Toshiya, Okayama Miki, Shitara Akiko, Mizoguchi Itaru, Takuma Taishin
Department of Biochemistry, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido, Japan; Department of Orthodontics, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido, Japan.
J Investig Clin Dent. 2014 Nov;5(4):266-74. doi: 10.1111/jicd.12049. Epub 2013 Jun 24.
The periodontal ligament (PDL) receives mechanical stress (MS) from dental occlusion or orthodontic tooth movement. Mechanical stress is thought to be a trigger for remodeling of the PDL and alveolar bone, although its signaling mechanism is still unclear. So we investigated the effect of MS on adenosine triphosphate (ATP) release and extracellular signal-regulated kinases (ERK) phosphorylation in PDL cells.
Mechanical stress was applied to human PDL cells as centrifugation-mediated gravity loading. Apyrase, Ca(2+)-free medium and purinergic receptor agonists and antagonists were utilized to analyze the contribution of purinergic receptors to ERK phosphorylation.
Gravity loading and ATP increased ERK phosphorylation by 5 and 2.5 times, respectively. Gravity loading induced ATP release from PDL cells by tenfold. Apyrase and suramin diminished ERK phosphorylation induced by both gravity loading and ATP. Under Ca(2+)-free conditions the phosphorylation by gravity loading was partially decreased, whereas ATP-induced phosphorylation was unaffected. Receptors P2Y4 and P2Y6 were prominently expressed in the PDL cells.
Gravity loading induced ATP release and ERK phosphorylation in PDL fibroblasts, and ATP signaling via P2Y receptors was partially involved in this phosphorylation, which in turn would enhance gene expression for the remodeling of PDL tissue during orthodontic tooth movement.
牙周膜(PDL)受到来自牙合或正畸牙齿移动的机械应力(MS)。尽管其信号传导机制仍不清楚,但机械应力被认为是牙周膜和牙槽骨重塑的触发因素。因此,我们研究了机械应力对牙周膜细胞中三磷酸腺苷(ATP)释放和细胞外信号调节激酶(ERK)磷酸化的影响。
以离心介导的重力加载对人牙周膜细胞施加机械应力。使用Apyrase、无钙培养基以及嘌呤能受体激动剂和拮抗剂来分析嘌呤能受体对ERK磷酸化的作用。
重力加载和ATP分别使ERK磷酸化增加了5倍和2.5倍。重力加载使牙周膜细胞的ATP释放增加了10倍。Apyrase和苏拉明减少了由重力加载和ATP诱导的ERK磷酸化。在无钙条件下,重力加载诱导的磷酸化部分降低,而ATP诱导的磷酸化不受影响。P2Y4和P2Y6受体在牙周膜细胞中显著表达。
重力加载诱导牙周膜成纤维细胞中ATP释放和ERK磷酸化,并且通过P2Y受体的ATP信号传导部分参与了这种磷酸化,这反过来会增强正畸牙齿移动过程中牙周膜组织重塑的基因表达。