Up-regulation of the endoplasmic reticulum stress-response in periodontal disease
Up-regulation of the endoplasmic reticulum stress-response in periodontal disease
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DOI：
10.1016/j.cca.2008.12.007
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发表时间：
2009-03-01
影响因子：
5
通讯作者：
Yamazaki, Kazuhisa
中科院分区：
文献类型：
--
作者：
Domon, Hisanori;Takahashi, Naoki;Yamazaki, Kazuhisa
背景资料：内质网（ER）应激是在各种条件下（如感染和衰老）通过激活未折叠蛋白反应（UPR）途径引起的细胞反应。UPR可能通过诱导细胞凋亡和激活核因子-κ B（NF-κ B B）（一种促炎细胞因子的转录因子）而与牙周病的发病机制相关。然而，ER应激与牙周病的关系尚不明确。方法：采用实时荧光定量聚合酶链反应和免疫组织化学方法检测牙周组织中UPR相关分子的表达。并与牙周炎进行比较。用大肠杆菌脂多糖（LPS）刺激巨噬细胞，分析其基因表达。结果：UPR相关基因和HSP 60在牙周炎组织中的表达水平明显高于牙龈炎组织。而牙龈卟啉单胞菌的LPS对E.结论：炎症反应可能对牙周炎患者的UPR反应有重要影响。考虑到牙周炎的组织学性质以及UPR与NF-κ B B介导的炎症反应之间的联系，B细胞中的ER应激可能是牙周病的另一种病理机制。(C)2008 Elsevier B. V.保留所有权利。
Background: Encloplasmic reticulum (ER) stress is the cell response by activation of the unfolded protein response (UPR) pathway in a variety of conditions such as infection and aging. The UPR may be associated with the pathogenesis of periodontal disease because of the induction of apoptosis and activation of nuclear factor-kappa B (NF-kappa B), a transcription factor for pro-inflammatory cytokines. However, the relationship between ER stress and periodontal disease is yet to be determined.Methods: The expression of UPR-related molecules was analyzed by real-time polymerase chain reaction and immunohistochemistry. respectively and compared between gingivitis and periodontitis. The gene expressions were also analyzed for macrophages stimulated with lipopolysaccharides (LPS) from Escherichia coli (E. coli), and Porphyromonas gingivalis (P. gingivalis) or IFN-gamma.Results: The expression levels of UPR-related genes and HSP60 were significantly higher in periodontitis compared with gingivitis lesions. However, LPS from P. gingivalis but not E. coli or IFN-gamma failed to up-regulate the gene expression in macrophage.Conclusions: An inflammatory response may have profound effect on the UPR response, particularly in periodontitis patients. Considering the histological nature of periodontitis and the link between UPR and inflammatory responses via NF-kappa B, ER stress in B cells could be another pathological mechanism underlying periodontal disease. (C) 2008 Elsevier B.V. All rights reserved.