Nakamura Toshiaki, Hasegawa-Nakamura Kozue, Sakoda Kenji, Matsuyama Takashi, Noguchi Kazuyuki
Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Japan.
Eur J Oral Sci. 2011 Oct;119(5):345-51. doi: 10.1111/j.1600-0722.2011.00850.x. Epub 2011 Aug 5.
The renin-angiotensin system is thought to be involved in inflammatory processes such as periodontitis. However, its precise role is still unclear. Therefore, in the present study the expression of the angiotensin II type 1 receptor (AT1R) was investigated in inflamed human gingival tissue, and the possible involvement of the AT1R in interleukin-1β (IL-1β)-induced interleukin-6 (IL-6) production by cultured human gingival fibroblasts (HGFs) was also studied. Immunohistochemical staining revealed that inflammatory cells and fibroblast-like cells were positive for the AT1R. However, in healthy gingival tissue, AT1R staining was very weak. The levels of AT1R mRNA and AT1R protein increased in HGFs after stimulation with IL-1β. The levels of IL-1β-induced IL6 mRNA and IL-6 protein were significantly reduced in AT1R gene-silenced HGFs compared with control HGFs. The data suggest that the AT1R may be involved in the regulation of gingival inflammation by modulating IL-1β-induced IL-6 production in HGFs.
肾素-血管紧张素系统被认为参与了诸如牙周炎等炎症过程。然而，其确切作用仍不清楚。因此，在本研究中，我们调查了血管紧张素II 1型受体（AT1R）在发炎的人牙龈组织中的表达情况，并且还研究了AT1R可能参与白细胞介素-1β（IL-1β）诱导培养的人牙龈成纤维细胞（HGFs）产生白细胞介素-6（IL-6）的情况。免疫组织化学染色显示，炎症细胞和成纤维样细胞的AT1R呈阳性。然而，在健康牙龈组织中，AT1R染色非常弱。在用IL-1β刺激后，HGFs中AT1R mRNA和AT1R蛋白的水平升高。与对照HGFs相比，在AT1R基因沉默的HGFs中，IL-1β诱导的IL6 mRNA和IL-6蛋白水平显著降低。数据表明，AT1R可能通过调节HGFs中IL-1β诱导的IL-6产生来参与牙龈炎症的调节。
