Terminal complement complex deposition on chondrocytes promotes premature senescence in age- and trauma-related osteoarthritis.

ABSTRACT:

Background

The complement system is locally activated after joint injuries and leads to the deposition of the terminal complement complex (TCC). Sublytic TCC deposition is associated with phenotypical alterations of human articular chondrocytes (hAC) and enhanced release of inflammatory cytokines. Chronic inflammation is a known driver of chondrosenescence in osteoarthritis (OA). Therefore, we investigated whether TCC deposition contributes to stress-induced premature senescence (SIPS) during aging in vivo and after ex vivo cartilage injury.

Methods

Femoral condyles of male 13-week-old and 72-week-old CD59-ko (higher TCC deposition), C6-deficient (insufficient TCC formation), and C57BL/6 (WT) mice were collected to assess age-related OA. Furthermore, macroscopi

SUBMITTER: Ruths L 

PROVIDER: S-EPMC11772281 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature