TNF-α-induced aquaporin 9 in synoviocytes from patients with OA and RA
Objectives. To determine whether aquaporins (AQPs) are expressed in the synovial tissues of patients with OA and RA, and to examine the patterns of expression in patients with and without hydrarthrosis. Methods. AQPs were detected in synovial tissue samples from patients with OA and RA using RT–PCR...
Saved in:
Published in | Rheumatology (Oxford, England) Vol. 49; no. 5; pp. 898 - 906 |
---|---|
Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Oxford University Press
01.05.2010
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Objectives. To determine whether aquaporins (AQPs) are expressed in the synovial tissues of patients with OA and RA, and to examine the patterns of expression in patients with and without hydrarthrosis. Methods. AQPs were detected in synovial tissue samples from patients with OA and RA using RT–PCR and immunohistochemistry. Fibroblast-like synoviocytes (FLSs) from patients with OA and RA were cultured and stimulated with TNF-α. The expression of AQPs in FLSs was examined using RT–PCR and western blot analyses and the function of aquaglyceroporins was examined by a glycerol uptake assay. Results. AQP1, -3 and -9 mRNAs were expressed in synovial tissues from patients with OA and RA. AQP1, -3 and -9 proteins were also detected by immunohistochemistry. AQP9 mRNA was expressed more strongly in the synovial tissues of OA patients with hydrarthrosis than those without. AQP9 mRNA and protein expression were strongly induced with TNF-α treatment in FLSs, whereas the expression of AQP1 and -3 mRNAs was not induced with TNF-α treatment. AQP9 as an aquaglyceroporin was induced by TNF-α. Conclusions. AQP9 mRNA was detected in synovial tissues from OA and RA patients with hydrarthrosis. AQP9 expression was strongly induced in FLSs with TNF-α. Although the functions of AQP1, -3 and -9 in synovial tissues remain to be elucidated, it suggested that AQP9 might be related to the pathogenesis of hydrarthrosis and inflammatory synovitis. |
---|---|
Bibliography: | ark:/67375/HXZ-MRMVHCBG-T istex:7B6DDE91F105D23B256C5918381EB742EC45FDF8 ArticleID:keq028 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1462-0324 1462-0332 |
DOI: | 10.1093/rheumatology/keq028 |