Carvacrol inhibits the progression of oral submucous fibrosis via downregulation of PVT1/miR-20a-5p-mediated pyroptosis

被引:1
作者
Yu, Cheng-Chia [1 ,2 ,3 ,4 ]
Hsieh, Pei-Ling [5 ]
Chao, Shih-Chi [1 ,6 ]
Liao, Yi-Wen [1 ,6 ]
Yu, Chuan-Hang [2 ,3 ,4 ]
Chueh, Pin Ju [7 ,8 ]
Peng, Chih-Yu [2 ,3 ,4 ]
Lee, Shiuan-Shinn [9 ]
机构
[1] Chung Shan Med Univ, Inst Oral Sci, Taichung, Taiwan
[2] Chung Shan Med Univ Hosp, Dept Dent, Taichung, Taiwan
[3] Chung Shan Med Univ, Sch Dent, 110 Sec1,Jianguo N Rd, Taichung 40201, Taiwan
[4] Chung Shan Med Univ, Oral Med Res Ctr, Taichung, Taiwan
[5] China Med Univ, Sch Med, Dept Anat, Taichung, Taiwan
[6] Chung Shan Med Univ Hosp, Dept Med Res, Taichung, Taiwan
[7] Natl Chung Hsing Univ, Inst Biomed Sci, Taichung, Taiwan
[8] Natl Chung Hsing Univ, Coll Med, Dept Postbaccalaureate Med, Taichung, Taiwan
[9] Chung Shan Med Univ, Coll Hlth care & management, Dept Publ Hlth, 110 Sec1,Jianguo N Rd, Taichung 40201, Taiwan
关键词
carvacrol; microRNA-20a; myofibroblast; oral submucous fibrosis; PVT1; MYOFIBROBLAST ACTIVITIES; PVT1; PROMOTES; CELLS; TRANSLOCATIONS; INFLAMMATION; FIBROBLASTS; GENERATION; MECHANISM; PATHWAYS;
D O I
10.1111/jcmm.70112
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Oral submucous fibrosis (OSF) is a precancerous condition in the oral cavity, which is closely related to the myofibroblast conversion of buccal mucosal fibroblasts (BMFs) after chronic consumption of areca nut. Emerging evidence suggests pyroptosis, a form of programmed cell death that is mediated by inflammasome, is implicated in persistent myofibroblast activation and fibrosis. Besides, numerous studies have demonstrated the effects of non-coding RNAs on pyroptosis and myofibroblast activities. Herein, we aimed to target key long non-coding RNA PVT1 with natural compound, carvacrol, to alleviate pyroptosis and myofibroblast activation in OSF. We first identified PVT1 was downregulated in the carvacrol-treated fBMFs and then demonstrated that myofibroblast features and expression of pyroptosis makers were all reduced in response to carvacrol treatment. Subsequently, we analysed the expression of PVT1 and found that PVT1 was aberrantly upregulated in OSF specimens and positively correlated with several fibrosis markers. After revealing the suppressive effects of carvacrol on myofibroblast characterisitcs and pyroptosis were mediated by repression of PVT1, we then explored the potential mechanisms. Our data showed that PVT1 may serve as a sponge of microRNA(miR)-20a to mitigate the myofibroblast activation and pyroptosis. Altogether, these findings indicated that the anti-fibrosis effects of carvacrol merit consideration and may be due to the attenuation of pyroptosis and myofibroblast activation by targeting the PVT1/miR-20a axis.
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页数:13
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