Expression and pathological effects of periostin in human osteoarthritis cartilage

Abstract

BackgroundOsteoarthritis (OA) is one of the most common joint diseases in elderly people, however, the underlying mechanism of OA pathogenesis is not completely clear. Periostin, the extracellular protein, has been shown by cDNA array analysis to be highly expressed in OA, but its function is not fully understood. The purpose of this study was to examine the expression and function of periostin in human OA.MethodsHuman cartilage and synovia samples were used for the analysis of periostin expression and function. The human cartilage samples were obtained from the knees of patients undergoing total knee arthroplasty as OA samples and from the femoral bone head of patients with femoral neck fracture as control samples. Quantitative RT-PCR, ELISA, and immunohistochemistry were used for analysis of periostin expression in cartilage and synovia. Human primary chondrocytes isolated from control cartilage were stimulated by periostin, and the alteration of OA related gene expression was examined using quantitative RT-PCR. Immunocytochemistry of p65 was performed for the analysis of nuclear factor kappa B (NFκB) activation.ResultsThe periostin mRNA was significantly higher in OA cartilage than in control cartilage. Immunohistochemical analysis of periostin showed that the main positive signal was localized in chondrocytes and their periphery matrix near the erosive area, with less immunoreactivity in deeper zones. There was positive correlation between Mankin score and periostin immunoreactivity. The periostin expression was also detected in the fibrotic cartilage and tissue of subchondral bone. In cultured human chondrocytes, periostin induced the expression of interleukin (IL)-6, IL-8, matrix metalloproteinase (MMP)-1, MMP-3, MMP-13, and nitric oxide synthase-2 (NOS2) in a dose- and time-dependent manner. The activation of NFκB signaling was recognized by the nuclear translocation of p65. Periostin-induced upregulation of these genes was suppressed by NFκB inactivation in chondrocytes.ConclusionPeriostin was upregulated in OA cartilage, and it may amplify inflammatory events and accelerate OA pathology.Electronic supplementary materialThe online version of this article (doi:10.1186/s12891-015-0682-3) contains supplementary material, which is available to authorized users.

Influence of Periostin on Synoviocytes in Knee Osteoarthritis

“…In addition, in some types of cells, periostin reportedly induces the expression of MMP family members (13,14). This induction and expression of matrix-degrading enzymes may function in tissues containing periostin, which is formed temporarily at the sites of damage to promote remodeling of the original tissue.…”

“…Periostin is considered to be an important structural mediator by balancing appropriate versus inappropriate tissue adaptation in response to insult/injury. Certain studies have shown that periostin is up-regulated in OA tissues (12)(13)(14). Previously, we reported that the periostin levels in synovial fluid were upregulated during the progression of OA in vivo, while in vitro experiments using human fibroblast-like synoviocytes suggested that addition of periostin mediated increased matrix metalloproteinase (MMP)-9 production (15).…”

Chondrocyte secretome: a source of novel insights and exploratory biomarkers of osteoarthritis

“…Expression of periostin was previously shown to be elevated in OA cartilage compared to normal, and located in the pericellular ECM close to damaged areas of cartilage [46,47]. Periostin is able to increase expression of IL-6, IL-8, MMP-1,-3,-13 and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4 by chondrocytes in vitro [46,47].…”

Evaluation of the chondroprotective action of N-acetylglucosamine in a rat experimental osteoarthritis model

“…Moreover, periostin induces inflammatory cytokines and MMPs via nuclear factor κB signaling, and promotes cartilage degeneration in patients with OA (30,31). Previous studies have demonstrated that the Postn expression is upregulated in the damaged cartilage of patients with knee OA (32)(33)(34). These observations suggest that GlcNAc has the potential to inhibit the degradation of type II collagen, as evidenced by the suppression of the level of C2C, a type II collagen degradation marker, by downregulating the expression of periostin.…”