Functional expression of α7 nicotinic acetylcholine receptors in human periodontal ligament fibroblasts and rat periodontal tissues

Functional expression of α7 nicotinic acetylcholine receptors in human periodontal ligament fibroblasts and rat periodontal tissues
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DOI:
10.1007/s00441-010-0949-9
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发表时间:
2010-03
影响因子:
3.6
通讯作者:
Xiao-jing Wang;Ying-Feng Liu;Qing-Yu Wang;Morito Tsuruoka;K. Ohta;Sheng-Xi Wu;M. Yakushiji;
Xiao-jing Wang;Ying-Feng Liu;Qing-Yu Wang;Morito Tsuruoka;K. Ohta;Sheng-Xi Wu;M. Yakushiji;
中科院分区:
生物学3区
文献类型:
--
作者:
Xiao-jing Wang;Ying-Feng Liu;Qing-Yu Wang;Morito Tsuruoka;K. Ohta;Sheng-Xi Wu;M. Yakushiji;

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吸烟是与慢性牙周炎相关的主要危险因素,但这种关系背后的机制在很大程度上是未知的。最近的报告提出,尼古丁通过非神经元细胞表达的烟碱乙酰胆碱受体(nAChR)发挥作用,在烟草相关的发病率中发挥重要作用。本研究旨在探讨α7 nAChR在牙周组织中的表达及其在牙周炎发病过程中是否通过调节IL-1β发挥作用。在体外,人牙周膜(PDL)细胞与10− 12 M尼古丁和/或10− 9 M α-银环蛇毒素(α-Btx)(α7 nAChR拮抗剂)一起培养。探讨α7 nAChR和IL-1β在PDL细胞中的表达及尼古丁/α-Btx对它们表达的影响。在体内建立大鼠实验性牙周炎模型,观察尼古丁/α-Btx对大鼠牙周炎发生、发展及α7 nAChR表达的影响。我们发现α7 nAChR在人牙周膜细胞和大鼠牙周组织中均有表达。尼古丁处理可显著增加α7 nAChR和IL-1β的表达,而α-Btx处理可部分抑制这一作用。本研究首次证实了α7 nAChR在人牙周膜细胞和大鼠牙周组织中的功能性表达。我们的研究结果可能有助于更好地了解吸烟、尼古丁和牙周炎之间的关系。
Tobacco smoking is the main risk factor associated with chronic periodontitis, but the mechanisms that underlie this relationship are largely unknown. Recent reports proposed that nicotine plays an important role in tobacco-related morbidity by acting through the nicotinic acetylcholine receptors (nAChRs) expressed by non-neuronal cells. The aim of this study was to investigate whether α7 nAChR was expressed in periodontal tissues and whether it functions by regulating IL-1β in the process of periodontitis. In vitro, human periodontal ligament (PDL) cells were cultured with 10−12M of nicotine and/or 10−9M of alpha-bungarotoxin (α-Btx), a α7 nAChR antagonist. The expression of α7 nAChR and IL-1β in PDL cells and the effects of nicotine/α-Btx administration on their expression were explored. In vivo, an experimental periodontitis rat model was established, and the effects of nicotine/α-Btx administration on expression of α7 nAChR and development of periodontitis were evaluated. We found that α7 nAChR was present in human PDL cells and rat periodontal tissues. The expressions of α7 nAChR and IL-1β were significantly increased by nicotine administration, whereas α-Btx treatment partially suppressed these effects. This study was the first to demonstrate the functional expression of α7 nAChR in human PDL cells and rat periodontal tissues. Our results may be pertinent to a better understanding of the relationships among smoking, nicotine, and periodontitis.