miR-522 Modulated the Expression of Proinflammatory Cytokines and Matrix Metalloproteinases Partly via Targeting Suppressor of Cytokine Signaling 3 in Rheumatoid Arthritis Synovial Fibroblasts

2018 ◽  
Vol 37 (4) ◽  
pp. 405-415 ◽  
Author(s):  
Xin Wang ◽  
Xuwei Si ◽  
Jiaying Sun ◽  
Lixia Yue ◽  
Jiajia Wang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Matrix Metalloproteinases ◽  
Proinflammatory Cytokines ◽  
Synovial Fibroblasts ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling

scholarly journals Shikonin Inhibits Inflammatory Response in Rheumatoid Arthritis Synovial Fibroblasts via lncRNA-NR024118

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Ke-ya Yang ◽  
Dong-liang Chen
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Response ◽  
Proinflammatory Cytokines ◽  
Synovial Fibroblasts ◽  
Bone Lesions ◽  
Socs3 Expression ◽  
Major Chemical ◽  
Cellular And Humoral Immunity ◽  
The Impact ◽  
Socs3 Protein

Background. Shikonin is a major chemical component of zicao that possesses anti-inflammatory properties and the ability to mediate cellular and humoral immunity, especially in rheumatoid arthritis (RA). We investigated the impact of shikonin on inflammatory response in RA synovial fibroblasts using the CAIA model.Methods. Severe polyarticular arthritis was induced in Balb/c female mice. Expressions of lncRNA-NR024118, SOCS3, proinflammatory cytokines, and MMPs were evaluated using RT-RCR. Histone acetylation and SOCS3 protein expression were assessed by ChIP assay and western blot, respectively.Results. Mice treated with shikonin showed an abrogation of soft tissue and bone lesions. Shikonin remarkably enhanced the expression of NR024118 and SOCS3 and suppressed the secretion and expression of IL-6, IL-8, and MMPs. Proliferation of cultured RA synovial fibroblasts in the presence of IL-1βwas also significantly inhibited by shikonin. Moreover, shikonin dose-dependently increased acetylation of histone H3 at the promoter of NR024118. Finally, NR024118 overexpression and interference significantly changed SOCS3 expression and NR024118 interference could reverse regulation of shikonin on SOCS3, proinflammatory cytokines, and MMPs expression level in MH7A cells.Conclusion. Our results reveal that, in the CAIA mouse model of RA, shikonin has disease modifying activity that is attributable to the inhibition of inflammatory response via lncRNA-NR024118.

scholarly journals Lunasin Inhibits Cell Proliferation via Apoptosis and Reduces the Production of Proinflammatory Cytokines in Cultured Rheumatoid Arthritis Synovial Fibroblasts

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Shaohui Jia ◽  
Shufang Zhang ◽  
Hong Yuan ◽  
Ning Chen
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Proliferation ◽  
Proinflammatory Cytokines ◽  
Synovial Cell ◽  
Synovial Fibroblasts ◽  
Nutritional Supplement ◽  
Luciferase Reporter ◽  
Drug Candidate ◽  
Matrix Metalloproteinase 3 ◽  
Anticancer Properties

Lunasin, a peptide with 43 amino acid residues and initially isolated and identified in soybean cotyledon, has gained extensive attention due to its anti-inflammatory and anticancer properties. However, its treatment efficacy on rheumatoid arthritis (RA) and corresponding mechanisms have not been reported. Herein, the synovial fibroblasts harvested and isolated from patients with RA were treated with lunasin at various concentrations to examine the proliferation, apoptosis status, and corresponding cell cycle of cultured RA synovial fibroblasts. Meanwhile, the underlying mechanisms of lunasin for RA treatment are explored through Western blot, real-time PCR, ELISA, and luciferase reporter assays. Lunasin significantly inhibited the proliferation and induced the apoptosis of cultured RA synovial fibroblasts. In addition, lunasin reduced the production of interleukin-6 (IL-6), IL-8, and matrix metalloproteinase-3 (MMP-3) and suppressed the activation of NF-κB in cultured RA synovial fibroblasts but did not reveal obvious modulation on the secretion and gene expression of MMP-1. Therefore, lunasin will have promising potential as a novel nutritional supplement or drug candidate for RA due to its potency of suppressing synovial cell proliferation and decreasing the production of proinflammatory cytokines and MMPs in synovial cells.

scholarly journals Increased Expression of Suppressor of Cytokine Signaling 1 mRNA in Patients With Rheumatoid Arthritis

2010 ◽  
Vol 26 (6) ◽  
pp. 290-298 ◽  
Author(s):  
Hua-Chen Chan ◽  
Liang-Yin Ke ◽  
Ching-Ching Liu ◽  
Lin-Li Chang ◽  
Wen-Chan Tsai ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling

scholarly journals Optimized “In Vitro” Culture Conditions for Human Rheumatoid Arthritis Synovial Fibroblasts

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Claudia Casnici ◽  
Donatella Lattuada ◽  
Noemi Tonna ◽  
Katia Crotta ◽  
Claudio Storini ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Proinflammatory Cytokines ◽  
Synovial Fibroblasts ◽  
In Vitro Studies ◽  
Tnf Alpha ◽  
Purinergic Signalling ◽  
Human Rheumatoid Arthritis ◽  
Cells Cultured

The composition of synovial fluid in rheumatoid arthritis (RA) is complex and strongly influences the microenvironment of joints and it is an inseparable element of the disease. Currently, “in vitro” studies are performed on RA cells cultured in the presence of either recombinant proinflammatory cytokines-conditioned medium or medium alone. In this study, we evaluated the use of synovial fluid, derived from RA patients, as optimal culture condition to perform “in vitro” studies on RA synovial fibroblasts. We observed that synovial fluid is more effective in inducing cell proliferation with respect to TNF-alpha or culture medium alone. Spontaneous apoptosis in fibroblasts was also decreased in response to synovial fluid. The expression of proinflammatory cytokines in the presence of synovial fluid was significantly elevated with respect to cells cultured with TNF-alpha or medium, and the overall morphology of cells was also modified. In addition, modulation of intracellular calcium dynamics elicited in response to synovial fluid or TNF-alpha exposure is different and suggests a role for the purinergic signalling in the modulation of the effects. These results emphasize the importance of using RA synovial fluid in “in vitro” studies involving RA cells, in order to reproduce faithfully the physiopathological environmental characteristic of RA joints.

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