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

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

  • Cell Death Dis. 2020 Jan 6;11(1):15. doi: 10.1038/s41419-019-2207-8.
Jie Du 1 2,  Ruifang Gao 3,  Yimei Wang 4,  Tivoli Nguyen 5,  Fang Yang 6,  Yongyan Shi 7,  Tianjing Liu 8,  Wang Liao 9,  Ran Li 3,  Fang Zhang 3,  Xuejun Ge 6,  Bin Zhao 10 11
Affiliations

Affiliations

  • 1 Department of Oral Medicine, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China. dj1243@hotmail.com.
  • 2 Institute of Biomedical Research, Shanxi Medical University, Taiyuan, Shanxi, China. dj1243@hotmail.com.
  • 3 Department of Oral Medicine, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China.
  • 4 Department of Endodontics, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China.
  • 5 Division of Biological Sciences, Department of Medicine, The University of Chicago, Chicago, IL, USA.
  • 6 Department of Periodontics, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China.
  • 7 Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
  • 8 Department of Pediatric Orthopedics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
  • 9 Department of Cardiology, Hainan General Hospital, Hainan Clinical Medicine Research Institution, Haikou, China.
  • 10 Department of Oral Medicine, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China. 18636666068@163.com.
  • 11 Department of prosthodontics, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China. 18636666068@163.com.
PMID: 31907356 DOI: 10.1038/s41419-019-2207-8
Abstract

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 Protein Kinase C δ (PKCδ) 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, PKCδ 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.

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