| Literature DB >> 29884447 |
Wei Zhou1, Li Su2, Xingyu Duan3, Xi Chen4, Aislinn Hays3, Satya Upadhyayula3, Juili Shivde3, Huizhi Wang3, Yong Li5, Dingming Huang4, Shuang Liang6.
Abstract
Periodontitis is one of the most prevalent inflammatory diseases, characterized by gingival inflammation and alveolar bone loss. MicroRNAs (MiRNAs) are important regulators of inflammation and involved in periodontitis pathogenesis. In this work, we studied the roles of microRNA-21 (miR-21) in periodontitis. MiR-21 is up-regulated in both periodontitis patients and the mice that induced with periodontitis. We tested the roles of miR-21 in the macrophages challenged by periodontitis pathogen Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS). MiR-21 expression is up-regulated in P. gingivalis LPS-stimulated macrophages. MiR-21 mimic inhibits the pro-inflammatory cytokine production by macrophages, while miR-21 deficiency elevates the production of pro-inflammatory cytokines. Moreover, absence of miR-21 promotes activation of nuclear factor-κB (NF-κB) in P. gingivalis LPS- stimulated cells. In a murine periodontitis model, ligation induced exacerbated gingival inflammation and alveolar bone loss in miR-21 deficient mice than their wild-type littermates. These results demonstrated the anti-inflammatory function of miR-21 in vitro and in vivo, indicating miR-21 could be an interventional target for the control of periodontitis.Entities:
Keywords: Bone loss; Inflammation; Macrophage; NF-κB; microRNA
Mesh:
Substances:
Year: 2018 PMID: 29884447 PMCID: PMC6182770 DOI: 10.1016/j.molimm.2018.05.008
Source DB: PubMed Journal: Mol Immunol ISSN: 0161-5890 Impact factor: 4.407