Exosomal transfer of osteoclast-derived miRNAs to chondrocytes contributes to osteoarthritis progression

Nat Aging. 2021 Apr;1(4):368-384. doi: 10.1038/s43587-021-00050-6. Epub 2021 Apr 15.

Abstract

Osteoarthritis (OA) is a prevalent aging-related joint disease lacking disease-modifying therapies. Here, we identified an upregulation of circulating exosomal osteoclast (OC)-derived microRNAs (OC-miRNAs) during the progression of surgery-induced OA in mice. We found that reducing OC-miRNAs by Cre-mediated excision of the key miRNA-processing enzyme Dicer or blocking the secretion of OC-originated exosomes by short interfering RNA-mediated silencing of Rab27a substantially delayed the progression of surgery-induced OA in mice. Mechanistically, the exosomal transfer of OC-miRNAs to chondrocytes reduced the resistance of cartilage to matrix degeneration, osteochondral angiogenesis and sensory innervation during OA progression by suppressing tissue inhibitor of metalloproteinase-2 (TIMP-2) and TIMP-3. Furthermore, systemic administration of a new OC-targeted exosome inhibitor (OCExoInhib) blunted the progression of surgery-induced OA in mice. We suggest that targeting the exosomal transfer of OC-miRNAs to chondrocytes represents a potential therapeutic avenue to tackle OA progression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chondrocytes
  • Mice
  • MicroRNAs* / genetics
  • Osteoarthritis* / genetics
  • Osteoclasts
  • Tissue Inhibitor of Metalloproteinase-2

Substances

  • MicroRNAs
  • Tissue Inhibitor of Metalloproteinase-2