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Regulation of tenascin-C expression by tumor necrosis factor-alpha in cultured human osteoarthritis chondrocytes.
J Rheumatol. 2008 Jan; 35(1):147-52.JR

Abstract

Expression of tenascin-C reappears in articular cartilage of persons with osteoarthritis (OA), while it is almost abolished in normal mature cartilage. Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, is upregulated in OA cartilage and is involved in the progression of OA, and stimulates tenascin-C expression in other types of cells. We investigated regulation of tenascin-C expression by TNF-alpha through nuclear factor-alphaB (NF-kappaB) in OA cartilage in vivo and in vitro.

METHODS

Human articular cartilages were obtained from patients with OA and immunofluorescence examination of tenascin-C and the activated RelA subunit was performed. Cultured chondrocytes isolated from human OA cartilage were treated with TNF-alpha and with SN50. Activation of RelA subunit of NF-kappaB was examined by immunolabeling. Changes in tenascin-C protein concentrations were determined by immunofluorescence of cells after monensin treatment and Western blot analysis of the cell lysates, and mRNA levels were analyzed by quantitative real-time polymerase chain reaction.

RESULTS

Increased intensity of tenascin-C staining was observed in the damaged cartilage compared with normal cartilage. Activated RelA staining in chondrocyte nuclei was prominent in tenascin-C-positive areas of OA cartilage. Treatment of cultured chondrocytes by TNF-alpha induced translocation of activated RelA to the nuclei, followed by upregulation of tenascin-C expression in both mRNA and protein. Treatment with SN50 inhibited increases of RelA and tenascin-C expression in chondrocytes.

CONCLUSION

TNF-alpha stimulated tenascin-C expression through NF-kappaB signaling with RelA activation in cultured OA chondrocytes, suggesting involvement of tenascin-C in OA cartilage remodeling.

Authors+Show Affiliations

Department of Orthopedic Surgery and Department of Pathology and Matrix Biology, Mie University Graduate School of Medicine, Mie, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18061975

Citation

Nakoshi, Yutaka, et al. "Regulation of tenascin-C Expression By Tumor Necrosis Factor-alpha in Cultured Human Osteoarthritis Chondrocytes." The Journal of Rheumatology, vol. 35, no. 1, 2008, pp. 147-52.
Nakoshi Y, Hasegawa M, Sudo A, et al. Regulation of tenascin-C expression by tumor necrosis factor-alpha in cultured human osteoarthritis chondrocytes. J Rheumatol. 2008;35(1):147-52.
Nakoshi, Y., Hasegawa, M., Sudo, A., Yoshida, T., & Uchida, A. (2008). Regulation of tenascin-C expression by tumor necrosis factor-alpha in cultured human osteoarthritis chondrocytes. The Journal of Rheumatology, 35(1), 147-52.
Nakoshi Y, et al. Regulation of tenascin-C Expression By Tumor Necrosis Factor-alpha in Cultured Human Osteoarthritis Chondrocytes. J Rheumatol. 2008;35(1):147-52. PubMed PMID: 18061975.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of tenascin-C expression by tumor necrosis factor-alpha in cultured human osteoarthritis chondrocytes. AU - Nakoshi,Yutaka, AU - Hasegawa,Masahiro, AU - Sudo,Akihiro, AU - Yoshida,Toshimichi, AU - Uchida,Atsumasa, Y1 - 2007/12/01/ PY - 2007/12/7/pubmed PY - 2008/3/12/medline PY - 2007/12/7/entrez SP - 147 EP - 52 JF - The Journal of rheumatology JO - J. Rheumatol. VL - 35 IS - 1 N2 - UNLABELLED: Expression of tenascin-C reappears in articular cartilage of persons with osteoarthritis (OA), while it is almost abolished in normal mature cartilage. Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, is upregulated in OA cartilage and is involved in the progression of OA, and stimulates tenascin-C expression in other types of cells. We investigated regulation of tenascin-C expression by TNF-alpha through nuclear factor-alphaB (NF-kappaB) in OA cartilage in vivo and in vitro. METHODS: Human articular cartilages were obtained from patients with OA and immunofluorescence examination of tenascin-C and the activated RelA subunit was performed. Cultured chondrocytes isolated from human OA cartilage were treated with TNF-alpha and with SN50. Activation of RelA subunit of NF-kappaB was examined by immunolabeling. Changes in tenascin-C protein concentrations were determined by immunofluorescence of cells after monensin treatment and Western blot analysis of the cell lysates, and mRNA levels were analyzed by quantitative real-time polymerase chain reaction. RESULTS: Increased intensity of tenascin-C staining was observed in the damaged cartilage compared with normal cartilage. Activated RelA staining in chondrocyte nuclei was prominent in tenascin-C-positive areas of OA cartilage. Treatment of cultured chondrocytes by TNF-alpha induced translocation of activated RelA to the nuclei, followed by upregulation of tenascin-C expression in both mRNA and protein. Treatment with SN50 inhibited increases of RelA and tenascin-C expression in chondrocytes. CONCLUSION: TNF-alpha stimulated tenascin-C expression through NF-kappaB signaling with RelA activation in cultured OA chondrocytes, suggesting involvement of tenascin-C in OA cartilage remodeling. SN - 0315-162X UR - https://www.unboundmedicine.com/medline/citation/18061975/Regulation_of_tenascin_C_expression_by_tumor_necrosis_factor_alpha_in_cultured_human_osteoarthritis_chondrocytes_ L2 - http://www.jrheum.org/cgi/pmidlookup?view=long&pmid=18061975 DB - PRIME DP - Unbound Medicine ER -