scholarly journals LAIR-1 shedding from human fibroblast-like synoviocytes in rheumatoid arthritis following TNF-α stimulation

2018 ◽  
Vol 192 (2) ◽  
pp. 193-205 ◽  
Author(s):  
Y. Zhang ◽  
S. Wang ◽  
H. Dong ◽  
X. Yi ◽  
J. Zhang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Human Fibroblast ◽  
Tnf Α ◽  
Fibroblast Like Synoviocytes

Down-regulation of microRNA-98 promoted apoptosis of TNF-α stimulated human fibroblast-like synoviocytes via up-regulating IL-10

Gene ◽  
2019 ◽  
Vol 706 ◽  
pp. 124-130 ◽  
Author(s):  
Zhizhou Li ◽  
Hongyu Chen ◽  
Fei Wang ◽  
Zaixin Wang ◽  
Qiheng Zhao ◽  
...  
Keyword(s):  
Human Fibroblast ◽  
Down Regulation ◽  
Tnf Α ◽  
Fibroblast Like Synoviocytes

scholarly journals Notch Signaling Mediates TNF-α-Induced IL-6 Production in Cultured Fibroblast-Like Synoviocytes from Rheumatoid Arthritis

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Zhijun Jiao ◽  
Wenhong Wang ◽  
Jie Ma ◽  
Shengjun Wang ◽  
Zhaoliang Su ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Notch Signaling ◽  
Target Gene ◽  
Cytokine Production ◽  
Notch Pathway ◽  
Mrna Levels ◽  
Secretase Inhibitor ◽  
Tnf Α ◽  
Functional Involvement ◽  
Fibroblast Like Synoviocytes

It has been reported that Notch family proteins are expressed in synovium tissue and involved in the proliferation of synoviocyte from rheumatoid arthritis (RA). The aim of this paper was to investigate whether Notch signaling mediated TNF-α-induced cytokine production of cultured fibroblast-like synoviocytes (FLSs) from RA. Exposure of RA FLSs to TNF-α(10 ng/ml) led to increase of Hes-1, a target gene of Notch signaling, and a marked upregulation of Notch 2, Delta-like 1, and Delta-like 3 mRNA levels. Blockage of Notch signaling by aγ-secretase inhibitor (DAPT) inhibited IL-6 secretion of RA FLSs in response to TNF-αwhile treatment with recombinant fusion protein of Notch ligand Delta-like 1 promoted such response. TNF-αstimulation also induced IL-6 secretion in OA FLSs; however, the Hes-1 level remained unaffected. Our data confirm the functional involvement of Notch pathway in the pathophysiology of RA FLSs which may provide a new target for RA therapy.

scholarly journals Activation of human fibroblast-like synoviocytes by uric acid crystals in rheumatoid arthritis

2011 ◽  
Vol 8 (6) ◽  
pp. 469-478 ◽  
Author(s):  
Da P Chen ◽  
Chun K Wong ◽  
Lai S Tam ◽  
Edmund K Li ◽  
Christopher WK Lam
Keyword(s):  
Rheumatoid Arthritis ◽  
Uric Acid ◽  
Human Fibroblast ◽  
Fibroblast Like Synoviocytes

scholarly journals The effect of nicotinamide adenine dinucleotide phosphate oxidase 4 on migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis

2020 ◽  
Author(s):  
Ha-Reum Lee ◽  
Su-Jin Yoo ◽  
Jinhyun Kim ◽  
In Seol Yoo ◽  
Chan Keol Park ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Migration ◽  
Adhesion Molecule ◽  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Migration And Invasion ◽  
Interleukin 17 ◽  
Tnf Α ◽  
Fibroblast Like Synoviocytes

Abstract Background: Reactive oxygen species (ROS) regulate the migration and invasion of fibroblast-like synoviocytes (FLS), which are key effector cells in rheumatoid arthritis (RA) pathogenesis. Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) induces ROS generation and consequently, enhances cell migration. Despite the important interrelationship between RA, FLS, and ROS, the effect of NOX4 on RA pathogenesis remains unclear. Methods: FLS isolated from RA (n=5) and osteoarthritis (OA, n=5) patients were stimulated with recombinant interleukin 17 (IL-17; 10 ng/ml) and tumor necrosis factor alpha (TNF-α; 10 ng/ml) for 1 h. Cell migration, invasion, adhesion molecule expression, vascular endothelial growth factor (VEGF) secretion, and ROS expression were examined. The mRNA and protein levels of NOX4 were analyzed by RT-qPCR and western blotting, respectively. The NOX4 inhibitor GLX351322 and NOX4 siRNA were used to inhibit NOX4 to probe the effect of NOX4 on these cellular processes. Results: Migration of RA FLS was increased 2.48-fold after stimulation with IL-17 and TNF-α, while no difference was observed for OA FLS. ROS expression increased in parallel with invasiveness of FLS following cytokine stimulation. When the expression of NOX was examined, NOX4 was significantly increased by 9.73-fold in RA FLS compared to unstimulated FLS. Following NOX4 inhibition, cytokine-induced vascular cell adhesion molecule 1 (VCAM1), VEGF, and migration and invasion capacity of RA FLS were markedly decreased to unstimulated levels. Conclusion: NOX4 is a key contributor to cytokine-enhanced migration and invasion via modulation of ROS, VCAM1, and VEGF in RA FLS.

Over-expression of PTEN attenuates the inflammation of fibroblast-like synoviocytes in rheumatoid arthritis

2020 ◽  
Author(s):  
Xiao-Feng Li ◽  
Qing-Qing Xu ◽  
Man-Wen Yang ◽  
He Chen ◽  
Su-Qin Yin ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Dna Methylation ◽  
Inflammatory Cytokines ◽  
Pten Expression ◽  
Over Expression ◽  
Tnf Α ◽  
And Migration ◽  
Fibroblast Like Synoviocytes ◽  
Pro Inflammatory Cytokines

Abstract Background: Rheumatoid arthritis (RA) is characterized by a tumor-like expansion of the synovium and the subsequent destruction of adjacent articular cartilage and bone. Recent studies have shown that phosphatase and tension homolog deleted on chromosome 10 (PTEN) might contribute to the survival of fibroblast-like synoviocytes (FLS) and the production of pro-inflammatory cytokines in RA.Methods : The expression was determined in RA and adjuvant-induced arthritis (AIA) synovial tissues by immunohistochemistry. FLSs were treatment with bpv, PTEN-RNAi or over-expression plasmid in RA and AIA. FLSs migration was assessed. The ad-PTEN was also injected into the knee of AIA in vivo. Chromatin Immunoprecipitation (ChIP) and Methylation-special PCR (MSP) assay were used to study the expression of PTEN mRNA in DNA methylation.Results : Down-regulated level of PTEN expression was observed in RA and AIA. Inhibition PTEN expression by bpv or PTEN-RNAi could promote the expression of pro-inflammatory cytokines, chemokines and migration of FLS with TNF-α in RA and AIA. Consistently, over-expression of PTEN reduced their low-expression of pro-inflammatory cytokines, chemokines and migration. Intra-articular injection of ad-PTEN in AIA knees dramatically reduced inflammatory and paw swelling in vivo. The ChIP and MSP assay has clearly detected the DNA methylation of PTEN was increased in FLS with TNF-α. Moreover, intraperitoneally injected 5-Aza in AIA also suppressed the inflammatory and paws swelling in vivo.Conclusions: Our findings suggest that over-expression PTEN attenuates the formation of pro-inflammatory cytokines, chemokines and migration of FLS, and it may be regulated by DNA methylation in the pathogenesis of RA.

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