例如:"lncRNA", "apoptosis", "WRKY"

MicroRNA-26a/b have protective roles in oral lichen planus.

Cell Death Dis. 2020 Jan 06;11(1):15
Jie Du 1 , Ruifang Gao 2 , Yimei Wang 3 , Tivoli Nguyen 4 , Fang Yang 5 , Yongyan Shi 6 , Tianjing Liu 7 , Wang Liao 8 , Ran Li 2 , Fang Zhang 2 , Xuejun Ge 5 , Bin Zhao 9
Jie Du 1 , Ruifang Gao 2 , Yimei Wang 3 , Tivoli Nguyen 4 , Fang Yang 5 , Yongyan Shi 6 , Tianjing Liu 7 , Wang Liao 8 , Ran Li 2 , Fang Zhang 2 , Xuejun Ge 5 , Bin Zhao 9
+ et al

[No authors listed]

Author information
  • 1 Institute of Biomedical Research, Shanxi Medical University, Taiyuan, Shanxi, China. dj1243@hotmail.com.
  • 2 Department of Oral Medicine, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China.
  • 3 Department of Endodontics, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China.
  • 4 Division of Biological Sciences, Department of Medicine, The University of Chicago, Chicago, IL, USA.
  • 5 Department of Periodontics, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China.
  • 6 Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
  • 7 Department of Pediatric Orthopedics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
  • 8 Department of Cardiology, Hainan General Hospital, Hainan Clinical Medicine Research Institution, Haikou, China.
  • 9 Department of prosthodontics, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China. 18636666068@163.com.

摘要


Oral lichen planus (OLP) is a kind of oral epithelial disorder featured with keratinocyte apoptosis and inflammatory reaction. The pathogenesis of OLP remains an enigma. Herein, we showed that the levels of miR-26a/b were robustly down-regulated in oral mucosal biopsies, serum and saliva in OLP patients compared with healthy control. Moreover, we found the binding sites of vitamin D receptor (VDR) in the promoter regions of miR-26a/b genes and proved that the induction of miR-26a/b was VDR dependent. The reduction of miR-26a/b expression was also detected in the oral epithelium of vitamin D deficient or VDR knockout mice. miR-26a/b inhibitors enhanced apoptosis and Type 1T helper (Th1) cells-related cytokines production in oral keratinocytes, whereas miR-26a/b mimics were protective. Mechanistically, we analyzed miRNA target genes and confirmed that miR-26a/b blocked apoptosis by directly targeting C δ which promotes cellular apoptotic processes. Meanwhile, miR-26a/b suppressed Th1-related cytokines secretion through targeting cluster of the differentiation 38 (CD38). In accordant with miR-26a/b decreases, and CD38 levels were highly elevated in OLP patients' samples. Taken together, our present investigations suggest that vitamin D/VDR-induced miR-26a/b take protective functions in OLP via both inhibiting apoptosis and impeding inflammatory response in oral keratinocytes.