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Published in: Rheumatology International 1/2004

01-01-2004 | Original Article

Interleukin-18 is regulated by G protein pathways and protein kinase signals in human fibroblasts

Authors: Marc K. Schuler, Wilhelm K. Aicher

Published in: Rheumatology International | Issue 1/2004

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Abstract

Interleukin-18 (IL-18) is a member of the IL-1 cytokine family and has proinflammatory activity. It has been detected in osteoarthritic (OA) and at higher levels in rheumatoid arthritic (RA) synovial tissue. Therefore we investigated major signal transduction pathways for their contribution to IL-18 expression. Here we report that cyclic adenosine monophosphate reduced and ionomycin increased IL-18 mRNA in RA synovial fibroblasts (SF) but not in OA SF. Moreover, activation of G-proteins by Mas-7 augmented IL-18 reverse transcriptase polymerase chain reaction signals in OA SF but not in RA SF. Specific protein kinase C activator phorbol myristate acetate reduced transcription and secretion of IL-18 in RA SF and OA SF. Staurosporine changed spontaneous IL-18 mRNA levels and increased the secretion of IL-18 protein. We conclude that G-protein activation and protein kinase C activation might partially be responsible for elevated IL-18 levels during RA.
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Metadata
Title
Interleukin-18 is regulated by G protein pathways and protein kinase signals in human fibroblasts
Authors
Marc K. Schuler
Wilhelm K. Aicher
Publication date
01-01-2004
Publisher
Springer-Verlag
Published in
Rheumatology International / Issue 1/2004
Print ISSN: 0172-8172
Electronic ISSN: 1437-160X
DOI
https://doi.org/10.1007/s00296-003-0321-4

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