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GM-CSF can exacerbate RA and elevated levels of this cytokine have been observed in synovial fluid from RA patients.
Increased levels of TIMP-1 have been observed in synovial fluid samples of RA as compared to psoriatic arthritis and are thus in agreement with our data [ 59].
Interestingly, overexpression of JUND (OA vs. RA) has not only been observed in synovial membranes, but also in proinflammatory synovial fibroblasts isolated from synovial tissue [ 92].
As for genetic variables, various expressions of growth factors and cytokines have been observed in synovial fluid and synovial tissues from patients with OA, within which resistin, an inflammatory cytokine, is one of those biomarkers [ 9– 12].
Activation of NF-κB has been observed in synovial cells from patients with RA [ 5] and results in the induction of proinflammatory genes such as tumor necrosis factor-α (TNF-α), IL-1β, IL-6, MMP-1, and MMP-3 in ex vivo synovial membrane cultures [ 6].
Similar(55)
The discovery, the authors add, could explain why small bubbles have be observed in synovial fluid even after knuckle-cracking.
eIn RA, the increase in antibody secreting cells is observed in synovial tissues.
Increased levels of Cx43 are observed in synovial biopsies from patients with OA.
In the normal group, very weak expression of FGF8 was observed in synovial cells but not in fibroblasts.
The expression of RANKL can be observed in synovial fibroblasts from patients with rheumatoid arthritis (RA) [ 5].
No overall changes were observed in synovial inflammation score or the presence of T cells, B cells or macrophages.
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