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A disintegrin and metalloproteinase with thrombospondin motifs 5 precursor (EC 3.4.24.-) (ADAM-TS 5) (ADAM-TS5) (ADAMTS-5) (A disintegrin and metalloproteinase with thrombospondin motifs 11) (ADAM-TS 11) (ADAMTS-11) (ADMP-2) (Aggrecanase-2) [ADAMTS11] [ADMP2]


Endoplasmic reticulum stress participates in the progress of senescence and apoptosis of osteoarthritis chondrocytes.

Endoplasmic reticulum stress (ERS) has been shown to participate in many disease pathologies. Recent reports have reported that ERS exists in human osteoarthritis (OA) chondrocytes. During OA, chondrocytes exhibit increased level of some senescence marker, such as senescence-associated β-galactosidase (SA β-gal) activity. However, the persistence and accumulation of senescent cells in various tissues can also impair function and have been involved in the pathogenesis of many age-related diseases, including OA. In this present study, we used IL-1β (10 ng/ml) to mimic OA chondrocytes and we found that IL-1β stimulated chondrocytes caused the increasing expression of ADAMTS5 and MMP13, decreasing COL2A1 expression, which were in accord with OA chondrocytes changes. Our data also showed that ERS is involved in the OA chondrocytes, SA β-gal activity significantly increases and inhibition of ERS can decrease the SA β-gal activity, apoptosis of OA chondrocytes and increase cell viability. These results help us to open new perspectives for the development of molecular-targeted treatment approaches and thus present an effective novel therapeutic approach for OA.

MeSH Terms

  • ADAMTS5 Protein
  • Apoptosis
  • Cartilage, Articular
  • Cell Survival
  • Cellular Senescence
  • Chondrocytes
  • Collagen Type II
  • Endoplasmic Reticulum Stress
  • Gene Expression Regulation
  • Humans
  • Interleukin-1beta
  • Matrix Metalloproteinase 13
  • Models, Biological
  • Osteoarthritis
  • Phenylbutyrates
  • Primary Cell Culture
  • Signal Transduction
  • beta-Galactosidase


  • Apoptosis
  • Endoplasmic reticulum stress
  • Interleukin-1β
  • Osteoarthritis chondrocytes
  • Senescence