The soluble terminal complement complex (SC5b-9) up-regulates osteoprotegerin expression and release by endothelial cells: Implications in rheumatoid arthritis

Claudio Tripodo, Lucia Rizzi, Tom E. Mollnes, Francesco Tedesco, Francesco Trotta, Gabriella Castellino, Arianna Gonelli, Fleur Bossi, Giorgio Zauli, Paola Secchiero, Federica Corallini

Risultato della ricerca: Article

19 Citazioni (Scopus)

Abstract

Objective. Complement activation products contribute to a large number of inflammatory diseases, including RA. We have investigated whether osteoprotegerin (OPG) may concur with the soluble terminal complement complex (SC5b-9) to the inflammatory cascade characterizing RA. Methods. Levels of SC5b-9 and OPG in the plasma and SF of patients with active RA were determined by ELISA. The presence of SC5b-9 and OPG in RA synovial lesions was analysed by immunohistochemistry. Cultured endothelial cells were used for in vitro leucocyte/endothelial cell adhesion assays. In addition, endothelial cells were exposed to SC5b-9 in order to evaluate the effects on the production of OPG protein, as well as the activation of the OPG promoter. Results. Patients affected by active RA are characterized by elevated levels of both SC5b-9 and OPG in plasma and/or SF. Of note, we have observed a co-localization of SC5b-9 and OPG in endothelial cells of post-capillary venules of RA synovial lesions. Data on endothelial cell cultures showed that exposure to SC5b-9 induced the up-regulation of OPG expression/release, stimulating the transcriptional activity of the OPG promoter, and synergized with TNF-α in up-regulating OPG production. Conclusions. Our findings demonstrate that SC5b-9 induces OPG production by endothelial cells and we propose that the SC5b-9-mediated up-regulation of OPG may be an important mechanism whereby complement contributes in promoting and/or enhancing the inflammation in RA. © The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved.
Lingua originaleEnglish
pagine (da-a)293-298
Numero di pagine6
RivistaRheumatology
Volume48
Stato di pubblicazionePublished - 2009

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Complement Membrane Attack Complex
Osteoprotegerin
Rheumatoid Arthritis
Up-Regulation
Endothelial Cells
Venules
Complement Activation
Cell Adhesion
Cultured Cells
Leukocytes

All Science Journal Classification (ASJC) codes

  • Rheumatology
  • Pharmacology (medical)

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The soluble terminal complement complex (SC5b-9) up-regulates osteoprotegerin expression and release by endothelial cells: Implications in rheumatoid arthritis. / Tripodo, Claudio; Rizzi, Lucia; Mollnes, Tom E.; Tedesco, Francesco; Trotta, Francesco; Castellino, Gabriella; Gonelli, Arianna; Bossi, Fleur; Zauli, Giorgio; Secchiero, Paola; Corallini, Federica.

In: Rheumatology, Vol. 48, 2009, pag. 293-298.

Risultato della ricerca: Article

Tripodo, C, Rizzi, L, Mollnes, TE, Tedesco, F, Trotta, F, Castellino, G, Gonelli, A, Bossi, F, Zauli, G, Secchiero, P & Corallini, F 2009, 'The soluble terminal complement complex (SC5b-9) up-regulates osteoprotegerin expression and release by endothelial cells: Implications in rheumatoid arthritis', Rheumatology, vol. 48, pagg. 293-298.
Tripodo, Claudio ; Rizzi, Lucia ; Mollnes, Tom E. ; Tedesco, Francesco ; Trotta, Francesco ; Castellino, Gabriella ; Gonelli, Arianna ; Bossi, Fleur ; Zauli, Giorgio ; Secchiero, Paola ; Corallini, Federica. / The soluble terminal complement complex (SC5b-9) up-regulates osteoprotegerin expression and release by endothelial cells: Implications in rheumatoid arthritis. In: Rheumatology. 2009 ; Vol. 48. pagg. 293-298.
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abstract = "Objective. Complement activation products contribute to a large number of inflammatory diseases, including RA. We have investigated whether osteoprotegerin (OPG) may concur with the soluble terminal complement complex (SC5b-9) to the inflammatory cascade characterizing RA. Methods. Levels of SC5b-9 and OPG in the plasma and SF of patients with active RA were determined by ELISA. The presence of SC5b-9 and OPG in RA synovial lesions was analysed by immunohistochemistry. Cultured endothelial cells were used for in vitro leucocyte/endothelial cell adhesion assays. In addition, endothelial cells were exposed to SC5b-9 in order to evaluate the effects on the production of OPG protein, as well as the activation of the OPG promoter. Results. Patients affected by active RA are characterized by elevated levels of both SC5b-9 and OPG in plasma and/or SF. Of note, we have observed a co-localization of SC5b-9 and OPG in endothelial cells of post-capillary venules of RA synovial lesions. Data on endothelial cell cultures showed that exposure to SC5b-9 induced the up-regulation of OPG expression/release, stimulating the transcriptional activity of the OPG promoter, and synergized with TNF-α in up-regulating OPG production. Conclusions. Our findings demonstrate that SC5b-9 induces OPG production by endothelial cells and we propose that the SC5b-9-mediated up-regulation of OPG may be an important mechanism whereby complement contributes in promoting and/or enhancing the inflammation in RA. {\circledC} The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved.",
author = "Claudio Tripodo and Lucia Rizzi and Mollnes, {Tom E.} and Francesco Tedesco and Francesco Trotta and Gabriella Castellino and Arianna Gonelli and Fleur Bossi and Giorgio Zauli and Paola Secchiero and Federica Corallini",
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T1 - The soluble terminal complement complex (SC5b-9) up-regulates osteoprotegerin expression and release by endothelial cells: Implications in rheumatoid arthritis

AU - Tripodo, Claudio

AU - Rizzi, Lucia

AU - Mollnes, Tom E.

AU - Tedesco, Francesco

AU - Trotta, Francesco

AU - Castellino, Gabriella

AU - Gonelli, Arianna

AU - Bossi, Fleur

AU - Zauli, Giorgio

AU - Secchiero, Paola

AU - Corallini, Federica

PY - 2009

Y1 - 2009

N2 - Objective. Complement activation products contribute to a large number of inflammatory diseases, including RA. We have investigated whether osteoprotegerin (OPG) may concur with the soluble terminal complement complex (SC5b-9) to the inflammatory cascade characterizing RA. Methods. Levels of SC5b-9 and OPG in the plasma and SF of patients with active RA were determined by ELISA. The presence of SC5b-9 and OPG in RA synovial lesions was analysed by immunohistochemistry. Cultured endothelial cells were used for in vitro leucocyte/endothelial cell adhesion assays. In addition, endothelial cells were exposed to SC5b-9 in order to evaluate the effects on the production of OPG protein, as well as the activation of the OPG promoter. Results. Patients affected by active RA are characterized by elevated levels of both SC5b-9 and OPG in plasma and/or SF. Of note, we have observed a co-localization of SC5b-9 and OPG in endothelial cells of post-capillary venules of RA synovial lesions. Data on endothelial cell cultures showed that exposure to SC5b-9 induced the up-regulation of OPG expression/release, stimulating the transcriptional activity of the OPG promoter, and synergized with TNF-α in up-regulating OPG production. Conclusions. Our findings demonstrate that SC5b-9 induces OPG production by endothelial cells and we propose that the SC5b-9-mediated up-regulation of OPG may be an important mechanism whereby complement contributes in promoting and/or enhancing the inflammation in RA. © The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved.

AB - Objective. Complement activation products contribute to a large number of inflammatory diseases, including RA. We have investigated whether osteoprotegerin (OPG) may concur with the soluble terminal complement complex (SC5b-9) to the inflammatory cascade characterizing RA. Methods. Levels of SC5b-9 and OPG in the plasma and SF of patients with active RA were determined by ELISA. The presence of SC5b-9 and OPG in RA synovial lesions was analysed by immunohistochemistry. Cultured endothelial cells were used for in vitro leucocyte/endothelial cell adhesion assays. In addition, endothelial cells were exposed to SC5b-9 in order to evaluate the effects on the production of OPG protein, as well as the activation of the OPG promoter. Results. Patients affected by active RA are characterized by elevated levels of both SC5b-9 and OPG in plasma and/or SF. Of note, we have observed a co-localization of SC5b-9 and OPG in endothelial cells of post-capillary venules of RA synovial lesions. Data on endothelial cell cultures showed that exposure to SC5b-9 induced the up-regulation of OPG expression/release, stimulating the transcriptional activity of the OPG promoter, and synergized with TNF-α in up-regulating OPG production. Conclusions. Our findings demonstrate that SC5b-9 induces OPG production by endothelial cells and we propose that the SC5b-9-mediated up-regulation of OPG may be an important mechanism whereby complement contributes in promoting and/or enhancing the inflammation in RA. © The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved.

UR - http://hdl.handle.net/10447/203581

M3 - Article

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