Full Papers
Vimentin fragments are potential markers of rheumatoid synovial fibroblasts
R. Vasko1, J.-H. Streich2, S. Blaschke3, G.A. Müller4, B. Mai5, M. Kostrzewa6, K. Sparbier7, P. Korsten8, S. Bohr9, H. Dihazi10
- Department of Nephrology and Rheumatology, University Medical Center, Göttingen, Germany.
- Department of Nephrology and Rheumatology, University Medical Center, Göttingen, Germany.
- Department of Nephrology and Rheumatology, University Medical Center, Göttingen, Germany.
- Department of Nephrology and Rheumatology, University Medical Center, Göttingen, Germany.
- Vitos Orthopaedic Clinic, Kassel, Germany.
- Bruker Daltonik GmbH, Bremen, Germany.
- Bruker Daltonik GmbH, Bremen, Germany.
- Department of Nephrology and Rheumatology, University Medical Center, Göttingen, Germany.
- Center for Engineering in Medicine, Harvard Medical School, Boston, MA, USA.
- Department of Nephrology and Rheumatology, University Medical Center, Göttingen, Germany. dihazi@med.uni-goettingen.de
CER8985
2016 Vol.34, N°3
PI 0513, PF 0520
Full Papers
Free to view
(click on article PDF icon to read the article)
PMID: 27049516 [PubMed]
Received: 18/09/2015
Accepted : 14/12/2015
In Press: 06/04/2016
Published: 30/05/2016
Abstract
OBJECTIVES:
To study the protein expression differences between primary fibroblasts explanted from synovial membranes of patients with rheumatoid arthritis (RA) and osteoarthritis (OA).
METHODS:
Fibroblast cultures were obtained from 10 patients with RA and 5 patients with OA. After two-dimensional gel electrophoresis, proteins were excised and identified using peptide mass fingerprint. Expression of selected proteins was subsequently examined by immunoblot. Furthermore, we examined the cellular lysates for the presence of citrullinated proteins.
RESULTS:
The study was designed to compare expression changes of the common proteins detected in all studied fibroblast cultures (i.e. detected in all patients samples). We totally identified 191 shared proteins between RA and OA fibroblasts. A significant difference was defined as at least 2-fold upregulation or 0.6-fold downregulation of protein expression. The most obvious alteration observed in RA was the appearance of several vimentin fragments not present in OA. We did not detect citrullinated proteins in lysates from RA fibroblasts. This corroborates the current assumption that fibroblasts are not able to citrullinate proteins by themselves and that invading macrophages play a central role in this process.
CONCLUSIONS:
We demonstrated that fibroblasts from patients with RA, despite being grown under identical conditions, preserve a particular feature and generate vimentin fragments not present in fibroblasts from OA. Elevated levels of different vimentin fragments have been recently reported in several rheumatic conditions. Further studies are needed to elucidate the pathogenic mechanisms induced by vimentin fragments in RA.
