scholarly journals Inflammatory Cytokines Stabilize SOXC Transcription Factors to Mediate the Transformation of Fibroblast-Like Synoviocytes in Arthritic Disease

2018 ◽  
Vol 70 (3) ◽  
pp. 371-382 ◽  
Author(s):  
Pallavi Bhattaram ◽  
George Muschler ◽  
Viktor Wixler ◽  
Véronique Lefebvre
Keyword(s):  
Transcription Factors ◽  
Inflammatory Cytokines ◽  
Arthritic Disease ◽  
Fibroblast Like Synoviocytes

scholarly journals Curcumin and Cancer

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2376 ◽  
Author(s):  
Giordano ◽  
Tommonaro
Keyword(s):  
Transcription Factors ◽  
Growth Factors ◽  
Cancer Therapy ◽  
Cell Signaling ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Biological Activities ◽  
Curcuma Longa ◽  
Cancer Development ◽  
Cell Signaling Pathways

Curcumin, a polyphenol extracted from Curcuma longa in 1815, has gained attention from scientists worldwide for its biological activities (e.g., antioxidant, anti-inflammatory, antimicrobial, antiviral), among which its anticancer potential has been the most described and still remains under investigation. The present review focuses on the cell signaling pathways involved in cancer development and proliferation, and which are targeted by curcumin. Curcumin has been reported to modulate growth factors, enzymes, transcription factors, kinase, inflammatory cytokines, and proapoptotic (by upregulation) and antiapoptotic (by downregulation) proteins. This polyphenol compound, alone or combined with other agents, could represent an effective drug for cancer therapy.

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.

Mechanisms of bone and cartilage destruction

2020 ◽  
pp. 85-94
Author(s):  
Ulrike Harre ◽  
Georg Schett
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Cytokines ◽  
Structural Damage ◽  
Current Knowledge ◽  
Joint Destruction ◽  
Cell Types ◽  
Significant Burden ◽  
Repair Mechanisms ◽  
And Cartilage ◽  
Fibroblast Like Synoviocytes

Structural damage of cartilage and bone tissue is a hallmark of rheumatoid arthritis (RA). The resulting joint destruction constitutes one of the major disease consequences for patients and creates a significant burden for the society. The main cells executing bone and cartilage degradation are osteoclasts and fibroblast-like synoviocytes, respectively. The function of both cell types is influenced by the immune system. In past decades, research has identified several mediators of structural damage, ranging from infiltrating immune cells and inflammatory cytokines to autoantibodies. These factors result in an inflammatory milieu in the affected joints, which leads to an increased development and function of osteoclasts and the transformation of fibroblast-like synoviocytes towards a highly migratory and destructive phenotype. In addition, repair mechanisms mediated by osteoblasts and chondrocytes are strongly impaired by the presence of pro-inflammatory cytokines. This article will review the current knowledge on the mechanisms of destruction of bone and cartilage in rheumatoid arthritis.

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.

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