<p>The biomechanical properties of the meniscus are involved in the pathogenesis of knee osteoarthritis (KOA), however, the biological role of a degenerated meniscus in KOA is unclear. This study examined the effects of degenerated meniscal tissue on articular chondrocytes using human meniscal tissues and articular chondrocytes obtained from 13 patients with KOA. Co-culture model and supernatant cell culture model were used and RNA sequencing, RT-qPCR and cell immunofluorescence staining were performed. The key finding of this study is that human degenerated meniscus alters expressions of OA-related genes and promotes productions of COX2 and MMP3 proteins in articular chondrocytes from KOA patients through paracrine effect. These findings suggest that degenerated human meniscal tissue induces inflammatory and degenerative changes in articular chondrocytes through a paracrine mechanism, potentially contributing to KOA pathogenesis.</p>

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Degenerated meniscus alters knee osteoarthritis-related gene expression in articular chondrocytes through paracrine mechanisms

  • Bo Guo,
  • Takashi Kanamoto,
  • Masaharu Aihara,
  • Satoshi Yamakawa,
  • Teruki Yokoyama,
  • Kosuke Ebina,
  • Hiroyuki Tanaka,
  • Ken Nakata

摘要

The biomechanical properties of the meniscus are involved in the pathogenesis of knee osteoarthritis (KOA), however, the biological role of a degenerated meniscus in KOA is unclear. This study examined the effects of degenerated meniscal tissue on articular chondrocytes using human meniscal tissues and articular chondrocytes obtained from 13 patients with KOA. Co-culture model and supernatant cell culture model were used and RNA sequencing, RT-qPCR and cell immunofluorescence staining were performed. The key finding of this study is that human degenerated meniscus alters expressions of OA-related genes and promotes productions of COX2 and MMP3 proteins in articular chondrocytes from KOA patients through paracrine effect. These findings suggest that degenerated human meniscal tissue induces inflammatory and degenerative changes in articular chondrocytes through a paracrine mechanism, potentially contributing to KOA pathogenesis.