scholarly journals Serum and urine levels of hyaluronic acid in rheumatoid arthritis.

Ensho ◽  
1996 ◽  
Vol 16 (2) ◽  
pp. 97-102
Author(s):  
Manabu Tanabe ◽  
Kae Ishiyama ◽  
Akira Suwa ◽  
Takashi Yamada ◽  
Shin-ichi Inada ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wei Zhang ◽  
Guoyu Yin ◽  
Heping Zhao ◽  
Hanzhi Ling ◽  
Zhen Xie ◽  
...  

AbstractIn inflamed joints, enhanced hyaluronic acid (HA) degradation is closely related to the pathogenesis of rheumatoid arthritis (RA). KIAA1199 has been identified as a hyaladherin that mediates the intracellular degradation of HA, but its extracellular function remains unclear. In this study, we found that the serum and synovial levels of secreted KIAA1199 (sKIAA1199) and low-molecular-weight HA (LMW-HA, MW < 100 kDa) in RA patients were significantly increased, and the positive correlation between them was shown for the first time. Of note, treatment with anti-KIAA1199 mAb effectively alleviated the severity of arthritis and reduced serum LMW-HA levels and cytokine secretion in collagen-induced arthritis (CIA) mice. In vitro, sKIAA1199 was shown to mediate exogenous HA degradation by attaching to the cell membrane of RA fibroblast-like synoviosytes (RA FLS). Furthermore, the HA-degrading activity of sKIAA1199 depended largely on its adhesion to the membrane, which was achieved by its G8 domain binding to ANXA1. In vivo, kiaa1199-KO mice exhibited greater resistance to collagen-induced arthritis. Interestingly, this resistance could be partially reversed by intra-articular injection of vectors encoding full-length KIAA1199 instead of G8-deleted KIAA119 mutant, which further confirmed the indispensable role of G8 domain in KIAA1199 involvement in RA pathological processes. Mechanically, the activation of NF-κB by interleukin-6 (IL-6) through PI3K/Akt signaling is suggested to be the main pathway to induce KIAA1199 expression in RA FLS. In conclusion, our study supported the contribution of sKIAA1199 to RA pathogenesis, providing a new therapeutic target for RA by blocking sKIAA1199-mediated HA degradation.



Crystals ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 321
Author(s):  
Shenghui Zhong ◽  
Peng Liu ◽  
Jinsong Ding ◽  
Wenhu Zhou

Methotrexate (MTX) is an anchor drug for the treatment of rheumatoid arthritis (RA); however, long-term and high-dose usage of MTX for patients can cause many side effects and toxic reactions. To address these difficulties, selectively delivering MTX to the inflammatory site of a joint is promising in the treatment of RA. In this study, we prepared MTX-PEI@HA nanoparticles (NPs), composed of hyaluronic acid (HA) as the hydrophilic negative electrical shell, and MTX-linked branched polyethyleneimine (MTX-PEI) NPs as the core. MTX-PEI@HA NPs were prepared in the water phase by a one-pot method. The polymeric NPs were selectively internalized via CD44 receptor-mediated endocytosis in the activated macrophages. In the in vivo mice mode study, treatment with MTX-PEI@HA NPs mitigated inflammatory arthritis with notable safety at a high dose of MTX. We highlight the distinct advantages of aqueous-synthesized NPs coated with HA for arthritis-selective targeted delivery, thus verifying MTX-PEI@HA NPs as a promising MTX-based nanoplatform for treatment of RA.



2016 ◽  
Vol 9 (1) ◽  
pp. 15-23
Author(s):  
SAID AL-DALAEN ◽  
AIMAN AL-QTAITAT ◽  
MOHAMMAD AL-RAWASHDEH ◽  
JIHAD ALZYOUD ◽  
AIMAN AL-MAATHADI


2005 ◽  
Vol 5 (1) ◽  
pp. 75-78 ◽  
Author(s):  
A.C. Nsonwu . ◽  
C.A.O. Usoro . ◽  
M.H. Etukudo . ◽  
I.N. Usoro .




Lupus ◽  
2020 ◽  
Vol 29 (4) ◽  
pp. 379-388 ◽  
Author(s):  
S Mirioglu ◽  
S Cinar ◽  
H Yazici ◽  
Y Ozluk ◽  
I Kilicaslan ◽  
...  

Objectives TNF-like weak inducer of apoptosis (TWEAK), monocyte chemoattractant protein-1 (MCP-1) and neutrophil gelatinase-associated lipocalin (NGAL) are proinflammatory cytokines/chemokines that are considered as potential biomarkers reflecting disease activity in systemic lupus erythematosus (SLE). In this study, we aimed to investigate the association of serum (s) and urine (u) levels of TWEAK, MCP-1 and NGAL with disease activity in both renal and extra-renal SLE. Methods Thirty active patients with SLE (15 renal and 15 extra-renal) were recruited. Thirty-one inactive patients with SLE (16 renal and 15 extra-renal), 14 patients with ANCA-associated vasculitis (AAV) all of whom had active renal involvement and 20 healthy volunteers were selected as control groups. Serum and urine levels of TWEAK, MCP-1 and NGAL were tested using ELISA. Results Serum and urine levels of TWEAK and NGAL were significantly higher in the active SLE group compared to the inactive SLE group (sTWEAK p = 0.005; uTWEAK p = 0.026; sNGAL p < 0.001; uNGAL p = 0.002), whilst no significant differences regarding serum and urine MCP-1 levels were observed ( p = 0.189 and p = 0.106, respectively). uTWEAK ( p = 0.237), sMCP-1 ( p = 0.141), uMCP-1 ( p = 0.206), sNGAL ( p = 0.419) and uNGAL ( p = 0.443) levels did not differ between patients with active renal and extra-renal SLE. Serum TWEAK was higher in patients with active renal SLE ( p = 0.006). There were no differences between active renal SLE and active renal AAV. Levels of all biomarkers were correlated with the SLE Disease Activity Index. Conclusion sTWEAK, uTWEAK, sNGAL and uNGAL are biomarkers showing disease activity in SLE. However, our results implicate that these biomarkers may not be specific for SLE, and can be elevated in patients with active renal involvement of AAV.



1975 ◽  
Vol 5 (3) ◽  
pp. 198-202 ◽  
Author(s):  
Barbara A. Peddie ◽  
Elsie Darin ◽  
Ross R. Bailey


2003 ◽  
Vol 6 (6) ◽  
pp. 547-551 ◽  
Author(s):  
Josh Weldin ◽  
Rhona Jack ◽  
Kathryn Dugaw ◽  
Raj P. Kapur

A 22-month-old boy, who regularly consumed the oral dietary supplement, quercetin, was suspected erroneously of having a catecholamine-producing tumor, based on elevated serum and urine levels of the dopamine metabolite, homovanillic acid (HVA). Subsequent studies of healthy adult volunteers showed that significant elevations in plasma HVA are a consequence of quercetin ingestion.



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