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MicroRNA-181b-5p modulates tumor necrosis factor-α-induced inflammatory responses by targeting interleukin-6 in cementoblasts.

Authors
  • Wang, Xiaoxuan1
  • Sun, Hualing1, 2
  • Liu, Huan1, 2
  • Ma, Li1
  • Jiang, Chenxi1
  • Liao, Haiqing1
  • Xu, Shihan1
  • Xiang, Junbo1, 2
  • Cao, Zhengguo1, 2
  • 1 The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China. , (China)
  • 2 Department of Periodontology, School and Hospital of Stomatology, Wuhan University, Wuhan, China. , (China)
Type
Published Article
Journal
Journal of Cellular Physiology
Publisher
Wiley (John Wiley & Sons)
Publication Date
Dec 01, 2019
Volume
234
Issue
12
Pages
22719–22730
Identifiers
DOI: 10.1002/jcp.28837
PMID: 31131439
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Tooth cementum is a bone-like mineralized tissue and serves as a microbial barrier against invasion and destruction. Cementum is also responsible for tooth stability and defending pulp from outside stimuli, which is formed by cementoblasts. Although it is crucial for periodontal and periapical diseases, the mechanisms underlying the pathophysiological changes of cementoblasts and their inflammatory responses remain unclear. MiR-181b is found to modulate vascular inflammation and endotoxin tolerance. In this study, miR-181b-5p was downregulated in tumor necrosis factor-α (TNF-α)-stimulated cementoblasts, whereas proinflammatory molecules increased. The mouse periapical lesions have similar results, which imitate an inflammatory environment for cementoblasts in vivo. The bioinformatics analysis and dual luciferase reporter assay suggested that miR-181b-5p targeted interleukin-6 (IL-6). Overexpressing miR-181b-5p negatively regulated IL-6 and proinflammatory chemokine. Western blot analysis and luciferase activity reporter assay verified that miR-181b-5p weakened the NF-κB activity. Hence, miR-181b-5p moderated proinflammatory chemokine production by targeting IL-6 in cementoblasts and NF-κB signaling pathway was involved. Furthermore, miR-181b-5p promoted cementoblast apoptosis, which may enhance the resolution of inflammation. Overall, our data revealed that miR-181b-5p was a negative regulator of TNF-α-induced inflammatory responses in cementoblasts. © 2019 Wiley Periodicals, Inc.

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