A comparative proteomics study of a synovial cell line stimulated with TNF‐α
Autor: | Tsuyoshi Iwasaki, Miki Karasaki, Mitsuyoshi Ueda, Seiji Shibasaki, Yumiko Takeda, Shunsuke Aburaya, Masayasu Kitano, Hajime Sano, Hironobu Morisaka, Wataru Aoki, Sachie Kitano |
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Rok vydání: | 2016 |
Předmět: |
rheumatoid arthritis
030203 arthritis & rheumatology 0301 basic medicine apoptosis gene ontology analysis Stimulation Biology Proteomics Molecular biology General Biochemistry Genetics and Molecular Biology comparative proteomics Pathogenesis 03 medical and health sciences TNF‐α 030104 developmental biology 0302 clinical medicine Synovial Cell Downregulation and upregulation Apoptosis Autophagy Protein 5 Tumor necrosis factor alpha Research Articles Research Article synovial cell line |
Zdroj: | FEBS Open Bio |
ISSN: | 2211-5463 |
DOI: | 10.1002/2211-5463.12049 |
Popis: | To elucidate the pathogenesis of rheumatoid arthritis (RA), we used proteomic analysis to determine the protein profile in a synovial cell line, MH7A, established from patients with RA. Proteins were extracted from MH7A cells that were or were not stimulated with tumor necrosis factor‐α (TNF‐α), and then analyzed on a liquid chromatography/mass spectrometry system equipped with a unique long monolithic silica capillary. On the basis of the results of this proteomic analysis, we identified 2650 proteins from untreated MH7A cells and 2688 proteins from MH7A cells stimulated with TNF‐α. Next, we selected 269 differentially produced proteins that were detected only under TNF‐α stimulation, and classified these proteins by performing gene ontology analysis by using DAVID as a functional annotation tool. In TNF‐α‐stimulated MH7A cells, we observed substantial production of plasminogen‐activator inhibitor 2 and apoptosis‐regulating proteins such as BH3‐interacting domain death agonist, autophagy protein 5, apolipoprotein E, and caspase‐3. These results indicate that the upregulation of plasminogen‐activator inhibitor 2 and apoptosis‐regulating proteins in synovial cells in response to TNF‐α stimulation might represent a predominant factor that contributes to the pathogenesis of RA. |
Databáze: | OpenAIRE |
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