Anti-Collagen Type II polyclonal antibody

Purpose: Chondrocyte extracellular matrix type II collagen and proteoglycans ensure an important compression-bearing structure in synovial joint. However, much more type I collagen is generated in osteoarthritis, which implies the presence of abnormal tensile strain in cartilage. We hypothesize that tensile stress influences chondrocyte phenotype at the cellular level, leading to potential osteoarthritis. Methods: Chondrocytes were stimulated with cyclic excessive tensile (10%) or mild tensile or compressive strain (5%) at 0.5 Hz, 3 h per day for 3 days. Chondrocyte morphology and matrix proteoglycans level was separately determined by Rhodamine phalloidin and toluldine blue staining. The expression of cartilage marker molecules was measured using quantitative reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assays. Results: Chondrocytes demonstrated significant fibroblastic morphology, reduced proliferation and increased apoptosis following exposure to 10% tensile strain. The 10% tensile strain group induced the lowest matrix proteoglycans level. It observably reduced the expression of COL2A1, Acan and SOX9, and increased COL1A1 expression level. The 5% tensile (5% compression) group, maintained the chondrocyte phenotype. Conclusions: The findings identified the effects of different magnitudes of tensile stress on chondrocyte phenotype compared to compressive strain. Further studies on cartilage biomechanical micro-environment might benefit from this study.

Sirtuins (SIRT1-7) are NAD(+)-dependent deacetylase/deacylases that regulate a wide variety of biological functions. Although the roles of sirtuins in cartilage homeostasis and cartilage diseases have been well studied, there is no information on the contribution of SIRT7 to cartilage homeostasis and osteoarthritis (OA) pathologies. Here, we demonstrate that Sirt7 knockout mice are resistant to the development of aging-associated OA and forced exercise-induced OA. Attenuation of Sirt7 in the murine chondrogenic cell line ATDC5 increased the deposition of a glycosaminoglycan-rich extracellular matrix and the mRNA expression of extracellular matrix components such as Col2a1 and Acan. Mechanistically, we found that SIRT7 suppressed the transcriptional activity of SOX9, which is an important transcription factor in chondrocytes, and that the enzymatic activity of SIRT7 was required for its function. Our results indicate that SIRT7 is a novel important regulator of cartilage homeostasis and OA development. (C) 2018 Elsevier Inc. All rights reserved.