Effect of Low-Level Laser Irradiation on CXCL13 Gene Expression in Rheumatoid Arthritis Rat Joints

  • Oshitani Toshiyuki
    Departments of Biochemistry and Molecular Biology, Nihon University School of Dentistry at Matsudo
  • Zhao Jian
    Departments of Biochemistry and Molecular Biology, Nihon University School of Dentistry at Matsudo
  • Kuboyama Noboru
    Molecular Pharmacology, Nihon University School of Dentistry at Matsudo
  • Abiko Yoshimitsu
    Departments of Biochemistry and Molecular Biology, Nihon University School of Dentistry at Matsudo Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo

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Rheumatoid arthritis (RA) is an inflammatory joint disorder, the progression of which leads to the destruction of cartilage and bone. Low-level laser irradiation (LLLI) is currently being evaluated for the treatment of RA, but the molecular mechanism underlying the effectiveness of LLLI in RA is unclear. B-cell-attracting chemokine-1 (CXCL13) is classified as a lymphoid chemokine and is a potent B-cell chemoattractant, leading to the local production of the autoantibody. The objective of this study was to determine whether LLLI decreased CXCL13 gene expression in joints of collagen-induced RA (CIA) rats. CIA caused swelling of rat joints, and LLLI significantly decreased the swelling. Total RNA was isolated from synovial membrane tissue of CIA rat joints with or without treatment from an 830 nm Ga-Al-As diode LLLI, and gene expression profiles were analyzed by DNA microarray (rat 41,000 genes). DNA microarray analysis showed that CXCL13 gene expression was increased in CIA tissue, and that LLLI significantly decreased the CIA-induced CXCL13 mRNA level. The reduction in CXCL13 gene expression was confirmed by reverse transcription polymerase chain reaction (RT-PCR) and real-time PCR. The findings suggest that decreased CXCL13 gene expression may be one of mechanisms involved in the reduction of inflammation in RA by LLLI.

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