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Abstract Number: 39

SDF-1 Induces Osteoclastogenesis in Rheumatoid Arthritis by Upregulating of RANKL Expression in Synovial Fibroblasts and CD4+ T Cells

Hae-Rim Kim1, Kyoung-Woon Kim2, Bo-Mi Kim1, Mi La Cho3 and Sang-Heon Lee4, 1Division of Rheumatology, Konkuk University School of Medicine, Seoul, South Korea, 2Conversant Research Consortium in Immunologic disease, The Catholic University of Korea, Seoul St. Mary's Hospital, Seoul, South Korea, 3Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea, Seoul, South Korea, 4Dept of Internal Medicine, Konkuk University Hospital, Seoul, South Korea

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Fibroblasts, osteoclasts and rheumatoid arthritis (RA)

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Session Information

Session Title: Biology and Pathology of Bone and Joint

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Stromal cell-derived factor (SDF)-1 is involved in bone destructive process in rheumatoid arthritis (RA) and bony metastasis in malignancy, through inducing angiogenesis, producing matrix-degrading enzymes and increasing survival and migration of osteoclasts. This study aimed to determine the mechanism of SDF-1 on osteoclastogenesis in RA.

Methods:

Synovial fibroblasts and CD4+ T cells were isolated from synovial tissues and peripheral blood of RA patients. The expression of SDF-1 and RANKL in the synovial tissues was evaluated using confocal microscopy. After synovial fibroblasts and CD4+ T cells were treated with rhSDF-1, the expression of RANKL mRNA was determined using real-time PCR. Osteoclastogenesis was analyzed in culture of human peripheral blood monocytes with SDF-1. Osteoclastogenesis was also determined after monocytes were co-cultured with rhSDF-1-stimulated RA synovial fibroblasts and CD4+ T cells.

Results: The expression of RANKL mRNA in RA synovial fibroblasts and CD4+ T cells was increased after SDF-1 stimulation. When RA synovial fibroblasts and CD4+ T cells were cultured with neutralizing antibody of TNF-a, the SDF-1-induced RANKL expression decreased, however, inhibition of IL-1b and IL-6 did not affect SDF-1-induced RANKL expression in both cell types. When CD14+ monocytes were cultured with SDF-1 in the absence of exogenous RANKL, the monocytes were differentiated into TRAP+ osteoclasts. Also, the monocytes were differentiated into TRAP+ osteoclasts when they were co-cultured with SDF-1-prestimulated RA synovial fibroblasts or CD4+T cells in the absence of exogenous RANKL.

Conclusion:

SDF-1 induced osteoclastogenesis by up-regulating RANKL expression in RA synovial fibroblasts and CD4+T cells and this is mediated by TNF-a. The axis of SDF-1 and RANKL is a potential therapeutic target for bony destructive process in RA.


Disclosure:

H. R. Kim,
None;

K. W. Kim,
None;

B. M. Kim,
None;

M. L. Cho,
None;

S. H. Lee,
None.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/sdf-1-induces-osteoclastogenesis-in-rheumatoid-arthritis-by-upregulating-of-rankl-expression-in-synovial-fibroblasts-and-cd4-t-cells/

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