scholarly journals Dual Role of Autophagy in Stress-Induced Cell Death in Rheumatoid Arthritis Synovial Fibroblasts

2013 ◽  
Vol 66 (1) ◽  
pp. 40-48 ◽  
Author(s):  
Masaru Kato ◽  
Caroline Ospelt ◽  
Renate E. Gay ◽  
Steffen Gay ◽  
Kerstin Klein
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Death ◽  
Synovial Fibroblasts ◽  
Dual Role

AB0071 Dual role of autophagy in stress-induced cell death in rheumatoid arthritis synovial fibroblasts

2013 ◽  
Vol 72 (Suppl 3) ◽  
pp. A807.2-A807
Author(s):  
M. Kato ◽  
C. Ospelt ◽  
B. A. Michel ◽  
R. E. Gay ◽  
S. Gay ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Death ◽  
Synovial Fibroblasts ◽  
Dual Role

The Role of Synovial Fibroblasts in Mediating Joint Destruction in Rheumatoid Arthritis

2005 ◽  
Vol 11 (5) ◽  
pp. 563-568 ◽  
Author(s):  
Ingmar Meinecke ◽  
Edita Rutkauskaite ◽  
Steffen Gay ◽  
Thomas Pap
Keyword(s):  
Rheumatoid Arthritis ◽  
Joint Destruction ◽  
Synovial Fibroblasts

scholarly journals Prostacyclin-IP signaling and prostaglandin E2-EP2/EP4 signaling both mediate joint inflammation in mouse collagen-induced arthritis

2006 ◽  
Vol 203 (2) ◽  
pp. 325-335 ◽  
Author(s):  
Tetsuya Honda ◽  
Eri Segi-Nishida ◽  
Yoshiki Miyachi ◽  
Shuh Narumiya
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Joint Inflammation ◽  
Synovial Fibroblasts ◽  
The Other ◽  
Receptor Subtype ◽  
Significant Suppression ◽  
Wild Type ◽  
Collagen Induced Arthritis

Prostaglandin (PG)I2 (prostacyclin [PGI]) and PGE2 are abundantly present in the synovial fluid of rheumatoid arthritis (RA) patients. Although the role of PGE2 in RA has been well studied, how much PGI2 contributes to RA is little known. To examine this issue, we backcrossed mice lacking the PGI receptor (IP) to the DBA/1J strain and subjected them to collagen-induced arthritis (CIA). IP-deficient (IP−/−) mice exhibited significant reduction in arthritic scores compared with wild-type (WT) mice, despite anti-collagen antibody production and complement activation similar to WT mice. IP−/− mice also showed significant reduction in contents of proinflammatory cytokines, such as interleukin (IL)-6 in arthritic paws. Consistently, the addition of an IP agonist to cultured synovial fibroblasts significantly enhanced IL-6 production and induced expression of other arthritis-related genes. On the other hand, loss or inhibition of each PGE receptor subtype alone did not affect elicitation of inflammation in CIA. However, a partial but significant suppression of CIA was achieved by the combined inhibition of EP2 and EP4. Our results show significant roles of both PGI2-IP and PGE2-EP2/EP4 signaling in the development of CIA, and suggest that inhibition of PGE2 synthesis alone may not be sufficient for suppression of RA symptoms.

Role of the Netrin System of Repellent Factors on Synovial Fibroblasts in Rheumatoid Arthritis and Osteoarthritis

2009 ◽  
Vol 22 (3) ◽  
pp. 715-722 ◽  
Author(s):  
T. Schubert ◽  
A. Denk ◽  
U. Mägdefrau ◽  
S. Kaufmann ◽  
P. Bastone ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fibroblasts

scholarly journals Lipid Peroxidation-Mediated Inflammation Promotes Cell Apoptosis through Activation of NF-κB Pathway in Rheumatoid Arthritis Synovial Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Geng Yin ◽  
Ying Wang ◽  
Xiao-min Cen ◽  
Min Yang ◽  
Yan Liang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Apoptosis ◽  
Inflammatory Responses ◽  
Synovial Fibroblasts ◽  
Systemic Autoimmune Disease ◽  
New Strategy ◽  
Significant Clinical Improvement ◽  
Rheumatoid Arthritis Synoviocytes ◽  
Initiation Of Therapy

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation of multiple joints. The central pathogenesis of RA is the proliferation of synovial fibroblasts in response to inflammatory cytokines. However, some of the targeted therapies for inflammation reactions do not display significant clinical improvement after initiation of therapy. Thus, the relationship between inflammatory responses and RA therapy is still incompletely understood. In the present study, we proposed to determine whether enhanced inflammations may lead to cell apoptosis in rheumatoid arthritis synoviocytes. Our results indicated that products of lipid peroxidations, 4-HNE, may induce synovial intrinsic inflammations by activating NF-κB pathways and it may lead to cell apoptosis. Pharmacological inhibition of NF-κB activation may reduce the 4-HNE mediated inflammation responses and subsequent cell apoptosis. Our results may help to clarify the role of inflammations on RA development and imply that blocking NF-κB activation may be partly beneficial for human RA therapy. These findings might provide a mechanism-based rationale for developing new strategy to RA clinical therapy.

scholarly journals Dual role of poly(ADP‐ribose) glycohydrolase in the regulation of cell death in oxidatively stressed A549 cells

2009 ◽  
Vol 23 (10) ◽  
pp. 3553-3563 ◽  
Author(s):  
Katalin Erdélyi ◽  
Péter Bai ◽  
István Kovács ◽  
Éva Szabó ◽  
Gábor Mocsár ◽  
...  
Keyword(s):  
Cell Death ◽  
A549 Cells ◽  
Dual Role

CXCL10 and TRAIL Are Upregulated by TXNDC5 in Rheumatoid Arthritis Fibroblast-like Synoviocytes

2017 ◽  
Vol 45 (3) ◽  
pp. 335-340 ◽  
Author(s):  
Bing Xu ◽  
Jian Li ◽  
Changsun Wu ◽  
Chunyan Liu ◽  
Xinfeng Yan ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Synovial Fibroblasts ◽  
And Migration ◽  
Interfering Rna ◽  
Synovial Membranes ◽  
Necrosis Factor ◽  
Fibroblast Like Synoviocytes

Objective.Thioredoxin domain containing 5 (TXNDC5) is highly expressed in synovial membranes of rheumatoid arthritis (RA). Our study aimed to investigate the pathogenic role of TXNDC5 in RA.Methods.PCR arrays, CCK-8 assays, flow cytometry, and transwell migration assays were used to analyze cultured rheumatoid arthritis synovial fibroblasts (RASF).Results.Increased CXCL10 and tumor necrosis factor-related apoptosis-inducing ligand levels were detected in RASF transfected with anti-TXNDC5 small interfering RNA (siRNA), and decreased expression was detected in RASF transfected with TXNDC5-expressing plasmids. Significantly attenuated RASF proliferation and migration, and increased RASF apoptosis, were observed in the siRNA-transfected RASF.Conclusion.Downregulation of TXNDC5 could contribute to RASF antiangiogenic and proapoptotic features through the suppression of CXCL10 and TRAIL (tumor necrosis factor-related apoptosis-inducing ligand).

scholarly journals Inhibition of Synovial Macrophage Pyroptosis Alleviates Synovitis and Fibrosis in Knee Osteoarthritis

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Li Zhang ◽  
Runlin Xing ◽  
Zhengquan Huang ◽  
Nongshan Zhang ◽  
Li Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Knee Osteoarthritis ◽  
Synovial Fibroblasts ◽  
Vital Role ◽  
Aseptic Inflammation ◽  
Synovial Macrophage ◽  
The Right ◽  
Related Proteins ◽  
Sirius Red

Increasing evidence has shown that macrophage pyroptosis in different tissues participates in chronic aseptic inflammation and is related to tissue fibrosis. Our last studies also revealed the vital role of synovial fibroblast pyroptosis in the onset and development of knee osteoarthritis (KOA). In this study, we aimed to investigate whether synovial macrophage pyroptosis did occur and whether this form of cell death should be related to synovitis and fibrosis of KOA. In the synovial tissue of KOA model rats, we observed a decrease of caspase1, NLRP3, ASC, and GSDMD caused by macrophage depletion in both the mRNA and protein expressions. Besides, rats treated with the specific caspase1 inhibitor Ac-YVAD-CMK showed less inflammatory reaction and fibrosis, not only in the expression of proinflammatory factors IL-1β, IL-18, and HMGB1 and fibrosis markers TGF-β, PLOD2, COL1A1, and TIMP1 but also in the observation of HE staining, Sirius Red staining, and the transverse diameters of the right knees. Subsequently, we established an LPS+ATP-induced model in macrophages mimicking the inflammatory environment of KOA and inducing macrophage pyroptosis. Macrophages transfected with caspase1 siRNA showed reduced cell death; meanwhile, the relative expression of pyroptosis-related proteins were also downregulated. In addition, the level of fibrotic markers in synovial fibroblasts were significantly decreased after coculture with siRNA GSDMD-transfected macrophages. To conclude, synovial macrophage pyroptosis may occur in the pathological processes of KOA and inhibition of synovial macrophage pyroptosis alleviates synovitis and fibrosis in KOA model rats.

scholarly journals Dual Role of Inorganic Polyphosphate (POLYP) in the Regulation of Mitochondria-Dependent Cell Death

2017 ◽  
Vol 112 (3) ◽  
pp. 439a
Author(s):  
Maria de la Encarnacion Solesio Torregrosa ◽  
Mitchell Marta-Ariza ◽  
Fernando Goni ◽  
Evgeny V. Pavlov
Keyword(s):  
Cell Death ◽  
Dual Role ◽  
Inorganic Polyphosphate ◽  
Dependent Cell
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