Downregulation of miR-106b attenuates inflammatory responses and joint damage in collagen-induced arthritis

Rheumatology (Oxford). 2017 Oct 1;56(10):1804-1813. doi: 10.1093/rheumatology/kex233.

Abstract

Objective: miRNAs are small, signal-strand, non-coding RNAs that function in post-transcriptional regulation. We analysed the in vivo effect of miR-106b (miR-106b-5p) on inflammatory bone loss in CIA mice.

Methods: CIA mice are developed by injecting DAB/1 mice with bovine type II collagen containing Freund's adjuvant and then the in vivo effect of miR-106b is examined. On day 22, mice were given lentiviral negative control, lentiviral-mediated miR-106b mimics or lentiviral-mediated miR-106b inhibitor via orbital injection on a weekly basis. Morphological changes in the ankle joints were assessed via micro-CT and histopathology and cytokine expression levels were examined via immunohistochemical staining, ELISA or flow cytometric analysis. miR-106b and osteoclastic-related gene expression was evaluated via quantitative real-time PCR.

Results: CIA mice were found to have increased miR-106b expression and CIA-associated bone loss and inflammatory infiltration. miR-106b inhibitor treatment markedly decreased arthritis incidence and attenuated bone destruction and histological severity compared with the control group. Moreover, miR-106b inhibitor treatment suppressed RANK ligand (RANKL) expression, increased osteoprotegerin (OPG) expression and reduced the RANKL:OPG ratio in CIA mice. miR-106b inhibition also significantly decreased inflammatory mediator production in joint sections and reduced serum pro-inflammatory cytokine levels when compared with the control group. Additionally, miR-106b inhibition decreased tartrate-resistant acid phosphatase-positive cell numbers and suppressed murine bone marrow macrophage differentiation.

Conclusion: These findings indicate that miR-106b inhibition can ameliorate CIA-associated inflammation and bone destruction and thus may serve as a potential therapeutic for human RA treatment.

Keywords: collagen-induced arthritis; inflammation; joint destruction; miR-106b; rheumatoid arthritis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arthritis, Experimental / chemically induced
  • Arthritis, Experimental / drug therapy
  • Arthritis, Experimental / genetics*
  • Bone and Bones / metabolism
  • Bone and Bones / pathology*
  • Collagen Type II
  • Cytokines / blood
  • Down-Regulation*
  • Gene Expression Regulation / drug effects
  • Inflammation Mediators / physiology
  • Joints / metabolism
  • Joints / pathology*
  • Male
  • Mice
  • Mice, Inbred DBA
  • MicroRNAs / antagonists & inhibitors
  • MicroRNAs / metabolism*
  • Osteoclasts / metabolism
  • Osteoprotegerin / metabolism
  • RANK Ligand / metabolism
  • Real-Time Polymerase Chain Reaction

Substances

  • Collagen Type II
  • Cytokines
  • Inflammation Mediators
  • MicroRNAs
  • Mirn106 microRNA, mouse
  • Osteoprotegerin
  • RANK Ligand
  • Tnfrsf11b protein, mouse