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      류마티스 관절염 동물 모델에서 활막의RANKL/OPG mRNA 발현 비율 및 IL-17의 효과 = Synovial RANKL/OPG mRNA Ratio and Effect of IL-17in Experimental Rheumatoid Arthritis Model

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      https://www.riss.kr/link?id=A104758257

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      다국어 초록 (Multilingual Abstract)

      Objective: To investigate the synovial mRNA expression of receptor activator of NFκB (RANK), RANK ligand (RANKL), osteoprotegerin (OPG) and RANKL/OPG mRNA expression ratio, and to evaluate the effects of IL-17 in experimental rheumatoid arthritis (RA) model.
      Methods: After induction of collagen-induced arthritis (CIA) by type II collagen in DBA1 mice, mice were anesthetized at day 28 and a small aperture in the skin of the knee was performed. Mice, in which arthritis of knee was present, were selected and divided into 3 groups, and phosphate-buffered saline (PBS group), IL-17 (IL-17 group) or anti-IL-17 monoclonal antibody (anti-IL-17 group) was injected to both knee joint at day 28 and 32. At day 35, mice were sacrificed and synovium of knee joints were isolated. Synovial mRNA expression of RANKL, RANK and OPG was assessed by real-time RT-PCR and immunohistochemical stain.
      Results: Synovial RANKL and RANK mRNA expressions were significantly different among IL-17, PBS, anti-IL-17 and normal group (IL-17>PBS>anti-IL-17>normal group), and synovia OPG mRNA expressions in PBS, IL-17 and anti-IL-17 group were significantly high than those in normal group, however, there was no significant difference among IL-17, PBS and anti-IL-17 group. RANKL/OPG mRNA ratio was significantly different among these groups (IL-17>PBS>anti-IL-17>normal group). In immunohistochemical stain, RANKL, RANK and OPG-positive cells were expressed at synovium.
      Conclusion: Synovial RANKL/OPG mRNA ratio was enhanced in CIA, and IL-17 induced higher RANKL/OPG ratio in the synovium of CIA, which was blocked by anti-IL-17 antibody. These results suggest that RANKL/OPG mRNA ratio play an important roles on bone destruction, and IL-17 may be actively involved in bone destruction by enhancing RANKL/OPG ratio in CIA model.
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      Objective: To investigate the synovial mRNA expression of receptor activator of NFκB (RANK), RANK ligand (RANKL), osteoprotegerin (OPG) and RANKL/OPG mRNA expression ratio, and to evaluate the effects of IL-17 in experimental rheumatoid arthritis (RA...

      Objective: To investigate the synovial mRNA expression of receptor activator of NFκB (RANK), RANK ligand (RANKL), osteoprotegerin (OPG) and RANKL/OPG mRNA expression ratio, and to evaluate the effects of IL-17 in experimental rheumatoid arthritis (RA) model.
      Methods: After induction of collagen-induced arthritis (CIA) by type II collagen in DBA1 mice, mice were anesthetized at day 28 and a small aperture in the skin of the knee was performed. Mice, in which arthritis of knee was present, were selected and divided into 3 groups, and phosphate-buffered saline (PBS group), IL-17 (IL-17 group) or anti-IL-17 monoclonal antibody (anti-IL-17 group) was injected to both knee joint at day 28 and 32. At day 35, mice were sacrificed and synovium of knee joints were isolated. Synovial mRNA expression of RANKL, RANK and OPG was assessed by real-time RT-PCR and immunohistochemical stain.
      Results: Synovial RANKL and RANK mRNA expressions were significantly different among IL-17, PBS, anti-IL-17 and normal group (IL-17>PBS>anti-IL-17>normal group), and synovia OPG mRNA expressions in PBS, IL-17 and anti-IL-17 group were significantly high than those in normal group, however, there was no significant difference among IL-17, PBS and anti-IL-17 group. RANKL/OPG mRNA ratio was significantly different among these groups (IL-17>PBS>anti-IL-17>normal group). In immunohistochemical stain, RANKL, RANK and OPG-positive cells were expressed at synovium.
      Conclusion: Synovial RANKL/OPG mRNA ratio was enhanced in CIA, and IL-17 induced higher RANKL/OPG ratio in the synovium of CIA, which was blocked by anti-IL-17 antibody. These results suggest that RANKL/OPG mRNA ratio play an important roles on bone destruction, and IL-17 may be actively involved in bone destruction by enhancing RANKL/OPG ratio in CIA model.

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      참고문헌 (Reference)

      1 "Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand" 96 : 3540-3545, 1999

      2 "Treatment with neutralizing anti-murine interleukin-17 antibody after the onset of collagen-induced arthritis reduces jont inflammation,cartilage destruction,and bone erosion" 50 : 650-659, 2004

      3 "The ratio fo messenger RNA levels of receptor activator of nuclear factor κB ligand to osteoprotegerin correlated with bone remodeling in normal human cancellous bone but not in osteoarthritis" 16 : 1015-1027, 2001

      4 "The osteoclast differentiation factor osteoprotegerin-ligand is essential for mammary gland development" 103 : 41-50, 2000

      5 "TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal kinase in T cells" 272 : 25190-25194, 1997

      6 "Synovial tissue in rheumatoid arthritis is a source of osteoclast differentiation factor" 43 : 250-258, 2000

      7 "Synovial fluid macrophages are capable of osteoclast formation and resorption" 208 : 35-43, 2006

      8 "Synovial fibroblasts promote osteoclast formation by RANKL in a novel model of spontaneous arthritis" 52 : 3257-3268, 2005

      9 "Skeletal changes in osteoportegerin and receptor activator of nuclear factor κB ligand mRNA levels in primary hyperparathyroidism:effects of parathyroidectomy and association with bone metabolism" 35 : 256-265, 2004

      10 "Reduction of joint inflammation and bone erosion in rat adjuvant arthritis by treatment with interleukin-17 receptor IgG1 Fc fusion protein" 46 : 802-805, 2002

      1 "Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand" 96 : 3540-3545, 1999

      2 "Treatment with neutralizing anti-murine interleukin-17 antibody after the onset of collagen-induced arthritis reduces jont inflammation,cartilage destruction,and bone erosion" 50 : 650-659, 2004

      3 "The ratio fo messenger RNA levels of receptor activator of nuclear factor κB ligand to osteoprotegerin correlated with bone remodeling in normal human cancellous bone but not in osteoarthritis" 16 : 1015-1027, 2001

      4 "The osteoclast differentiation factor osteoprotegerin-ligand is essential for mammary gland development" 103 : 41-50, 2000

      5 "TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal kinase in T cells" 272 : 25190-25194, 1997

      6 "Synovial tissue in rheumatoid arthritis is a source of osteoclast differentiation factor" 43 : 250-258, 2000

      7 "Synovial fluid macrophages are capable of osteoclast formation and resorption" 208 : 35-43, 2006

      8 "Synovial fibroblasts promote osteoclast formation by RANKL in a novel model of spontaneous arthritis" 52 : 3257-3268, 2005

      9 "Skeletal changes in osteoportegerin and receptor activator of nuclear factor κB ligand mRNA levels in primary hyperparathyroidism:effects of parathyroidectomy and association with bone metabolism" 35 : 256-265, 2004

      10 "Reduction of joint inflammation and bone erosion in rat adjuvant arthritis by treatment with interleukin-17 receptor IgG1 Fc fusion protein" 46 : 802-805, 2002

      11 "Receptor activator of nuclear factor κB ligand ratio is increased in severe osteolysis" 163 : 2021-2031, 2003

      12 "Quantification of mRNA levels in joint capsule and articular cartilage of the murine knee joint by RT-PCR.Kinetics of stromelysin and IL-1 mRNA levels during arthritis" 16 : 197-205, 1997

      13 "Pathogenesis of bone erosions in rheumatoid arthritis" 12 : 195-199, 2000

      14 "Osteoprotegerin:a novel secreted protein involved in the regulation of bone density" 89 : 309-319, 1997

      15 "Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation" 93 : 165-176, 1998

      16 "Osteoprotegerin and RANKL regulated bone resroption,density,geometry and strength" 5 : 618-625, 2005

      17 "OPGL is a key regulator of osteoclastogenesis,lymphocyte development and lymph- node organogenesis" 397 : 315-323, 1999

      18 "Modulation of osteoclast diffrentiation and function by the new members of the tumor necrosis factor receptor and ligand families" 20 : 345-357, 1999

      19 "Involvement of receptor activator of nuclear factor κB ligand/osteoclast differentiation factor in osteoclastogenesis from synoviocytes in rheumatoid arthritis" 43 : 259-269, 2000

      20 "Interleukin-7 stimulates osteoclast formation by up-regulating the T-cell production of soluble osteoclastogenic cytokines" 96 : 1873-1878, 2000

      21 "Interleukin-6 and soluble interleukin-6 receptor in the synovial fluids from rheu-matoid arthritis patients are responsible for osteoclast-like cell formation" 11 : 88-95, 1996

      22 "Interleukin-1β and tumor necrosis factor-α,but not interleukin-6,stimulate osteoprotegerin ligand gene expression in human osteoblastic cells" 25 : 255-259, 1999

      23 "Interleukin-17 synergises with tumor necrosis factor α to induce cartilage destruction in vitro" 61 : 870-876, 2002

      24 "Increased RANKL/OPG mRNA ratio in iliac crest bone biopsies from women with hip fracture" 76 : 90-97, 2005

      25 "IL-17 promotes bone erosion in murine collagen-induced arthritis through loss of the receptor activator of NF-κB ligand/osteoprotegerin balance" 170 : 2655-2662, 2003

      26 "IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis" 103 : 1345-1352, 1999

      27 "IL-1-independent role of IL-17 in synovial inflammation and joint destruction during collagen-induced arthritis" 167 : 1004-1013, 2001

      28 "Human osteoclast formation and bone resorption by monocytes and synovial macrophages in rheumatoid arthritis" 55 : 3597-3602, 1996

      29 "Expression of osteoclast differentiation factor at sites of bone erosion in collagen-induecd arthritis" 43 : 821-826, 2000

      30 "Diverse roles of the tumor necrosis factor family member TRANCE deficiency and partial rescue by a lymphocyte-expressed TRANCE transgene" 97 : 10905-10910, 2000

      31 "Chondrocytes and osteoclasts at subchondral sites of erosions in the rheumatoid joint" 27 : 968-75, 1984

      32 "Changes in serum receptor activator of nuclear factor-κB ligand,osteoprotegerin,and interleukin-6 levels in patients with glucocorticoid- induced osteoporosis treated with human parathyroid hormone" 89 : 3332-3336, 2004

      33 "A new mechanism of bone destruction in rheumatoid arthritis:synovial fibroblasts induce osteoclastogenesis" 240 : 279-286, 1997

      34 "A homologue of the TNF receptor and its ligand enhance T-cell growth and dendritic-cell function" 390 : 175-179, 1997

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      연월일 이력구분 이력상세 등재구분
      2027 평가예정 재인증평가 신청대상 (재인증)
      2021-01-01 평가 등재학술지 유지 (재인증) KCI등재
      2018-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2016-03-09 학회명변경 영문명 : The Korean Rheumatism Association -> Korean College of Rheumatology KCI등재
      2015-04-03 학술지명변경 외국어명 : The Journal of the Korean Rheumatism Association -> Journal of Rheumatic Diseases KCI등재
      2015-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2006-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2005-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2003-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.1 0.1 0.08
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.08 0.09 0.242 0.09
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