Expression of autophagy-associated proteins in rat dental irreversible pulpitis

被引:27
作者
Qi, Shengcai [1 ]
Qian, Jun [2 ]
Chen, Fubo [1 ]
Zhou, Peng [2 ]
Yue, Jing [1 ]
Tang, Fengqin [1 ]
Zhang, Yiming [1 ]
Gong, Shiqiang [3 ]
Shang, Guangwei [1 ]
Cui, Chun [3 ]
Xu, Yuanzhi [1 ]
机构
[1] Tongji Univ, Dept Stomatol, Shanghai Peoples Hosp 10, Sch Med, 301 Yanchang Rd, Shanghai 200072, Peoples R China
[2] Nanjing Med Univ, Jiangsu Key Lab Oral Dis, Affiliated Hosp Stomatol, Nanjing 210029, Jiangsu, Peoples R China
[3] Huazhong Univ Sci & Technol, Ctr Stomatol, Tongji Hosp, Tongji Med Coll, 1095 Jie Fang Ave, Wuhan 430030, Hubei, Peoples R China
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
autophagy; irreversible pulpitis; rat dental pulpitis model; INNATE; INFLAMMATION; IMMUNITY; CELLS; LIPOPOLYSACCHARIDE; DIFFERENTIATION; ACTIVATION; HYPOXIA; INJURY; PROBE;
D O I
10.3892/mmr.2019.9944
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Autophagy serves an important role in numerous diseases, as well as in infection and inflammation. Irreversible pulpitis (IP) is one of the most common inflammatory endodontic diseases, and autophagy has been reported to regulate IP in vitro. However, the level of autophagy in the IP pathogenic process in vivo remains unknown. The aim of the current study was, thus, to investigate the levels of autophagy-associated proteins in rats with IP in vivo. A rat dental IP model was successfully constructed, and five different time points (0, 1, 3, 5 and 7 days) were investigated. The levels of the autophagy-related 5 (ATG5), ATG7, light chain 3 (LC3) and Beclin-1 proteins exhibited a time-dependent increase in rats with IP, whereas the levels of mammalian target of rapamycin and p62/sequestosome 1 were decreased. In addition, the levels of ATG proteins were specifically increased in odontoblasts and microvascular endothelial cells in pulpitis tissue. Based on these findings, autophagy may serve an important role in IP, and the present study data provide a new insight into the IP pathogenesis and treatment.
引用
收藏
页码:2749 / 2757
页数:9
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