TY - JOUR
T1 - Expression and pathological effects of periostin in human osteoarthritis cartilage
AU - Chijimatsu, Ryota
AU - Kunugiza, Yasuo
AU - Taniyama, Yoshiaki
AU - Nakamura, Norimasa
AU - Tomita, Tetsuya
AU - Yoshikawa, Hideki
N1 - Funding Information:
Yasuo Kunugiza is supported by a Grant-in-Aid for Scientific Research (C) (Grant No 24592260) and a Grant of the Osaka Medical Research Foundation for Incurable Diseases. Tetsuya Tomita is supported by a Grant-in-Aid for challenging Exploratory Research (Grant No 256706460). The authors thank Mari Shinkawa for technical support.
Publisher Copyright:
© 2015 Chijimatsu et al.
PY - 2015/8/21
Y1 - 2015/8/21
N2 - Background: 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. Methods: 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. Results: 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. Conclusion: Periostin was upregulated in OA cartilage, and it may amplify inflammatory events and accelerate OA pathology.
AB - Background: 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. Methods: 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. Results: 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. Conclusion: Periostin was upregulated in OA cartilage, and it may amplify inflammatory events and accelerate OA pathology.
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U2 - 10.1186/s12891-015-0682-3
DO - 10.1186/s12891-015-0682-3
M3 - Article
C2 - 26289167
AN - SCOPUS:84939488180
SN - 1471-2474
VL - 16
JO - BMC Musculoskeletal Disorders
JF - BMC Musculoskeletal Disorders
IS - 1
M1 - 215
ER -
