Yin Wei, Dong Ming, Ye Dandan, Liu Qicheng, Liu Shuo, Shi Chun, Bai Hua, Wang Qian, Yang Xue, Wang Lina, Niu Weidong
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine (Ministry of Education), School & Hospital of Stomatology, Wuhan University, Wuhan 430079, China; Department of Biomedical Data Science, Geisel School of Medicine at Dartmouth College, One Medical Center Drive, Lebanon, NH 03756, USA.
School of Stomatology, Dalian Medical University, Dalian 116044, China.
Sci Bull (Beijing). 2020 Jun 15;65(11):951-957. doi: 10.1016/j.scib.2019.12.006. Epub 2019 Dec 10.
Although the role of cathepsin C (Cat C) in inflammation is gradually being elucidated, its function in periapical periodontitis, which is one of the most common infectious diseases worldwide, has not been studied. This study evaluated a surgically-induced model of periapical periodontitis in cathepsin C (Cat C) knock-down (KD) mice, which was constructed with a tetracycline operator, to evaluate the role of Cat C in the pathogenesis and progression of periapical periodontitis. Our results showed, for the first time, that there was a statistically significant increase in the expression of Cat C as periapical periodontitis progressed; this increase started from 1 week after surgery and reached a peak at 3 weeks after surgery, before gradually decreasing. The volume of periapical bone resorption in Cat C KD mice was significantly smaller than that in wild-type mice at 3 and 4 weeks after surgery (P<0.05). Inflammatory cell infiltration into the apical tissues of wild-type mice was also significantly higher than that of Cat C KD mice. The expression of receptor activator of nuclear factor-κB ligand (RANKL) in wild-type mice was also higher than that in Cat C KD mice. The difference in the number of osteoclasts in the apical area between the two groups was statistically significant after 2 weeks. Correlation analysis showed that there was a significant correlation between Cat C and RANKL expression (r= 0.835). Therefore, our data indicated that Cat C promoted the apical inflammation and bone destruction in mice.
尽管组织蛋白酶C（Cat C）在炎症中的作用正逐渐被阐明，但其在根尖周炎（全球最常见的传染病之一）中的功能尚未得到研究。本研究评估了用四环素操纵子构建的组织蛋白酶C（Cat C）基因敲低（KD）小鼠的手术诱导根尖周炎模型，以评估Cat C在根尖周炎发病机制和进展中的作用。我们的结果首次表明，随着根尖周炎的进展，Cat C的表达在统计学上有显著增加；这种增加从手术后1周开始，在手术后3周达到峰值，然后逐渐下降。在手术后3周和4周，Cat C KD小鼠的根尖骨吸收体积显著小于野生型小鼠（P<0.05）。野生型小鼠根尖组织中的炎性细胞浸润也显著高于Cat C KD小鼠。野生型小鼠中核因子κB受体激活剂配体（RANKL）的表达也高于Cat C KD小鼠。两组根尖区域破骨细胞数量的差异在2周后具有统计学意义。相关性分析表明，Cat C与RANKL表达之间存在显著相关性（r=0.835）。因此，我们的数据表明，Cat C促进了小鼠的根尖炎症和骨破坏。
