Section of Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany.
Department of Orthodontics, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany.
Mediators Inflamm. 2017;2017:4786170. doi: 10.1155/2017/4786170. Epub 2017 Dec 6.
Cathepsin S is a cysteine protease and regulator of autophagy with possible involvement in periodontitis. The objective of this study was to investigate whether cathepsin S is involved in the pathogenesis of periodontal diseases. Human periodontal fibroblasts were cultured under inflammatory and infectious conditions elicited by interleukin-1 and , respectively. An array-based approach was used to analyze differential expression of autophagy-associated genes. Cathepsin S was upregulated most strongly and thus further studied at gene and protein levels. , gingival tissue biopsies from rats with ligature-induced periodontitis and from periodontitis patients were also analyzed at transcriptional and protein levels. Multiple gene expression changes due to interleukin-1 and were observed . Both stimulants caused a significant cathepsin S upregulation. A significantly elevated cathepsin S expression in gingival biopsies from rats with experimental periodontitis was found , as compared to that from control. Gingival biopsies from periodontitis patients showed a significantly higher cathepsin S expression than those from healthy gingiva. Our findings provide original evidence that cathepsin S is increased in periodontal cells and tissues under inflammatory and infectious conditions, suggesting a critical role of this autophagy-associated molecule in the pathogenesis of periodontitis.
组织蛋白酶 S 是一种半胱氨酸蛋白酶和自噬调节剂,可能参与牙周炎的发生。本研究旨在探讨组织蛋白酶 S 是否参与牙周病的发病机制。将人牙周成纤维细胞在白细胞介素-1 和 分别诱导的炎症和感染条件下进行培养。采用基于阵列的方法分析自噬相关基因的差异表达。组织蛋白酶 S 的上调最为显著,因此在基因和蛋白水平上进一步进行了研究。还分析了结扎诱导牙周炎大鼠和牙周炎患者牙龈组织活检的转录和蛋白水平。观察到白细胞介素-1 和 引起的多个基因表达变化。两种刺激物均导致组织蛋白酶 S 的显著上调。与对照组相比,在实验性牙周炎大鼠的牙龈活检中发现组织蛋白酶 S 的表达明显升高。牙周炎患者的牙龈活检组织中组织蛋白酶 S 的表达明显高于健康牙龈。我们的研究结果提供了原始证据,表明组织蛋白酶 S 在炎症和感染条件下牙周细胞和组织中增加,提示该自噬相关分子在牙周炎发病机制中起关键作用。