The online version of this article (doi:10.1186/s12891-015-0682-3) contains supplementary material, which is available to authorized users.
The authors declare that they have no competing interests.
CR performed the study, analyzed, interpreted the data, and drafted the manuscript; KY contributed to the design of the study, prepared samples, and helped draft the manuscript; TY contributed to the design of the study and helped draft the manuscript; TT and NN contributed to the design of the study, prepared sample; YH contributed to the design of the study. All authors read and approved the manuscript.
Osteoarthritis (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.
Human 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.
The 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.
Periostin was upregulated in OA cartilage, and it may amplify inflammatory events and accelerate OA pathology.
Additional file 1: Primer list for qRT-PCR. (XLSX 10 kb)12891_2015_682_MOESM1_ESM.xlsx
Additional file 2: Periostin upregulated OA related genes in a similar trend among all donors. The same trend of periostin effects was observed in two other donors by qRT-PCR for cells (A) and ELISA for culture supernatant (B), although the endogenous expression of OA related catabolic, inflammatory, anabolic genes was different among donors. *, P < 0.05. (PDF 145 kb)12891_2015_682_MOESM2_ESM.pdf
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- Expression and pathological effects of periostin in human osteoarthritis cartilage
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