l-Glutathione enhances antioxidant capacity of hyaluronic acid and modulates expression of pro-inflammatory cytokines in human fibroblast-like synoviocytes

2016 ◽  
Vol 104 (8) ◽  
pp. 2071-2079 ◽  
Author(s):  
Kai-Chiang Yang ◽  
Chang-Chin Wu ◽  
Wei-Yu Chen ◽  
Shoichiro Sumi ◽  
Teng-Le Huang
Keyword(s):  
Hyaluronic Acid ◽  
Antioxidant Capacity ◽  
Inflammatory Cytokines ◽  
Human Fibroblast ◽  
Fibroblast Like Synoviocytes ◽  
Pro Inflammatory Cytokines

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.

scholarly journals IL-36γ in Enthesitis related Juvenile Idiopathic Arthritis and its association with disease activity.

2021 ◽  
Author(s):  
Sanjukta Majumder et al.
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Synovial Fluid ◽  
Disease Activity ◽  
Inflammatory Cytokines ◽  
Feedback Loop ◽  
Mononuclear Cells ◽  
Inflammatory Bowel ◽  
Fibroblast Like Synoviocytes ◽  
Pro Inflammatory Cytokines

IL-36 has been implicated in the pathogenesis of spondyloarthropathies (SpA) like psoriasis and inflammatory bowel disease. Enthesitis related arthritis (ERA) category of juvenile idiopathic arthritis is a form of juvenile SpA, however no data is available on the role of IL-36 in this disease. IL-36α, β, γ and IL-36R mRNA expression in blood and synovial fluid mononuclear cells and IL-36α, γ, IL-36Ra, IL-6 and IL-17 levels were measured in serum and synovial fluid (SF). IL-36γ production by fibroblast like synoviocytes (FLS) by pro-inflammatory cytokines and its effect on FLS was also studied.mRNA levels of IL-36α, IL-36γ and IL-36R were increased in PBMCs of ERA patients as compared to healthy controls however only IL-36γ was measurable in serum of one third of patients. In SFMCs, all 4 mRNA were detectable but were lower than RA patients. SF IL-36γ levels correlated with disease activity score (r=0.51, p< 0.0001), SF IL-6 (r=0.4,p= 0.0063) and IL-17 levels (r=0.57,p=0.0018). Pro-inflammatory cytokines increased expression of IL-36γ and IL-6 in FLS cultures. SFs from 5 ERA patients also increased expressions of IL-36γ and IL-6 in FLS which could be blocked by using IL-36Ra.This suggests that pro-inflammatory cytokines aid in upregulation of IL-36γ which in turn upregulates expression of IL-6. This might lead to a positive feedback loop of inflammation in ERA. Association of SF levels of IL-36γ with disease activity further supports this possibility. IL-36Ra based therapy may have a role in ERA.

scholarly journals Fibroblast-Like-Synoviocytes Mediate Secretion of Pro-Inflammatory Cytokines via ERK and JNK MAPKs in Ti-Particle-Induced Osteolysis

Materials ◽  
2020 ◽  
Vol 13 (16) ◽  
pp. 3628
Author(s):  
Ashish Ranjan Sharma ◽  
Supriya Jagga ◽  
Chiranjib Chakraborty ◽  
Sang-Soo Lee
Keyword(s):  
Inflammatory Cytokines ◽  
Wear Debris ◽  
Therapeutic Option ◽  
Underlying Mechanism ◽  
Early Response ◽  
Periprosthetic Osteolysis ◽  
Protein Levels ◽  
Living Tissues ◽  
Fibroblast Like Synoviocytes ◽  
Pro Inflammatory Cytokines

Biomaterials are designed to replace and augment living tissues in order to provide functional support to skeletal deformities. However, wear debris produced from the interfaces of metal implants initiates inflammatory bone loss, causing periprosthetic osteolysis. Lately, fibroblast-like synoviocytes (FLS) have been shown to play a role in wear-debris-induced osteolysis. Thus, here we have tried to understand the underlying mechanism of FLS involvement in wear-debris-induced osteolysis. Our results demonstrate that the effects of Ti particle (1:100 cell-to-Ti particle ratio) on FLS can induce Cox-2 expression and activate NFkB signaling. Moreover, the mRNA expression of pro-inflammatory cytokines such as IL-6, IL-8, IL-11, IL-1β, and TNFα was found to be elevated. However, among these pro-inflammatory cytokines, the mRNA and protein levels of only IL-6, IL-1β, and TNFα were found to be significantly higher. Ti particles activated extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinases (MAPKs) as an early response in FLS. Co-inhibition of ERK and JNK signaling pathways by their specific inhibitors (PD9805 and SP600125, respectively) resulted in the suppression of mRNA and protein levels of IL-6, IL-1β, and TNFα in FLS. Taken together, targeting ERK and JNK MAPKs in FLS might provide a therapeutic option for reducing the secretion of bone-resorbing pro-inflammatory cytokines, thus preventing periprosthetic osteolysis.

scholarly journals Effect of 1,25-(OH)2D3 on Proliferation of Fibroblast-Like Synoviocytes and Expressions of Pro-Inflammatory Cytokines through Regulating MicroRNA-22 in a Rat Model of Rheumatoid Arthritis

2017 ◽  
Vol 42 (1) ◽  
pp. 145-155 ◽  
Author(s):  
Ping Fan ◽  
Lan He ◽  
Nan Hu ◽  
Jing Luo ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Cytokines ◽  
Rat Model ◽  
Type Ii Collagen ◽  
Proliferation Inhibition ◽  
Blank Group ◽  
Mtt Method ◽  
Cox 2 ◽  
Fibroblast Like Synoviocytes ◽  
Pro Inflammatory Cytokines

Objective: This study aims to investigate the regulatory mechanism of 1,25-(OH)2D3 on the proliferation of fibroblast-like synoviocytes (FLS) and expressions of pro-inflammatory cytokines in rheumatoid arthritis (RA) rats via microRNA-22 (miR-22). Methods: A rat model of RA was established with a subcutaneous injection of type II collagen. After treated with different concentrations of 1,25-(OH)2D3 the proliferation of FLS was estimated by the MTT method, and the optimal concentration of 1,25-(OH)2D3 was selected for further experiments. Cell proliferation was detected by MTT. Cell cycle and apoptosis were analyzed by FCM. The IL-1β, IL-6, IL-8, and PGE2 protein expressions were determined by ELISA, and MMP-3, INOS, and Cox-2 mRNA expressions were measured by qRT-PCR. Results: The rat model of RA was successfully established. Compared with the blank group, the 1,25-(OH)2D3 and miR-22 inhibitors groups exhibited higher proliferation inhibition and apoptosis rates, lower levels of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and PGE2), and decreased mRNA expressions of MMP-3, INOS, and Cox-2. The miR-22 mimics group had lower proliferation inhibition and apoptosis rates, elevated expressions of pro-inflammatory cytokines and MMP-3, INOS, and Cox-2 than the blank group. In contrast to the 1,25-(OH)2D3 group, the proliferation inhibition and apoptosis rates were down-regulated, and the expressions of pro-inflammatory cytokines and MMP-3, INOS, and Cox-2 were up-regulated in the 1,25-(OH)2D3 + miR-22 mimics group. Conclusion: Our study demonstrated that 1,25-(OH)2D3 inhibits the proliferation of FLS and alleviates inflammatory response in RA rats by down-regulating miR-22.

scholarly journals In vitro Anti-Inflammatory Effects of Hyaluronic Acid in Ethanol-Induced Damage in Skin Cells

2011 ◽  
Vol 14 (3) ◽  
pp. 425 ◽  
Author(s):  
Manuela G Neuman ◽  
Radu M Nanau ◽  
Loida Oruña ◽  
Gabriel Coto
Keyword(s):  
Hyaluronic Acid ◽  
Inflammatory Cytokines ◽  
Chronic Wounds ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Separate Experiment ◽  
Mouse Fibroblasts ◽  
Skin Cells ◽  
The Media ◽  
Pro Inflammatory Cytokines

ABSTRACT - Ethyl alcohol (ethanol) is commonly applied in cosmetic and pharmaceutical preparations, as well as disinfectant for chronic wounds. Objective: The present study aimed to appraise physiological levels of ethanol-induced damage in skin cells in vitro and the possible repair by hyaluronic acid (HA). In addition, we aimed to establish cytokine-chemokine networks in the cellular media and the modulation of cytokines such as tumor necrosis factor-alpha (TNF-B), interferon-alpha (IFN-α), transforming growth factor-beta (TGF-B), interleukins (IL) such as IL1-B and IL-6, as well as matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP). Design and Methods: We treated human A431 epidermoid skin cells and mouse fibroblasts with ethanol at a concentration of 100 mM over 24 hours (h). A separate experiment looked at the effects of 2 consecutive treatments with 100 mM ethanol for 24 h each. HA obtained from umbilical cord excision was used at two concentration levels (2% and 4%) to determine its efficacy in the treatment. We measured cytotoxicity and cytokine networks in the media. Results: Treatment of cells with 100 mM ethanol increased cytotoxicity, as well as the release of pro-inflammatory cytokines into the culture medium. Conclusions: Ethanol may induce cytotoxicity in skin cells by enhancing the effects of pro-inflammatory cytokines. HA reduced the amount of pro-inflammatory cytokines released into the media both in human A431 epidermoid skin cells and in mouse fibroblasts. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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