Determinants of thromboxane biosynthesis in rheumatoid arthritis: Role of RAGE and oxidant stress

Ferrante, Elisabetta; Vazzana, Natale; Santilli, Francesca; Cicco, Maria Di; Lauriti, Ciro; Battista, L; Ciabattoni, Giovanni; Matteo, Luigi Di; Davı̀, Giovanni

doi:10.1016/j.freeradbiomed.2010.06.009

Cited by 19 publications

(13 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Moreover, TxA2 release was increased in peripheral blood leucocytes when cultured with RA synovial fluid exudates [ 38 , 39 ]. Recently, a study recruited 54 RA patients as well as 20 healthy subjects and found that the biosynthesis of TxA2 in RA patients was significantly higher than healthy controls [ 40 ], which is in agreement with our recent report for the first time showing that serum level of TxA2 is positively correlated with 28-joint disease activity (DAS28) score of patients with RA [ 19 ]. Additionally, we also found that in RA fibroblast-like synoviocytes (RA-FLS), COX-2 effects can be mainly mediated by TxA2, and the mRNA expression of COX-2 is regulated by TxA2 action [ 11 ].…”

Section: Role Of the Cox-2/txa2 Pathway In The Pathogenesis Of Rasupporting

confidence: 86%

“…The limitations and side effects of these drugs are considered to be, at least in part, due to lack of the effects on the biosynthesis of COX-2-derived TxA2 [ 11 ]. In support of this view, it is found that treatment of RA patients with anti-TNF-α agents, belonging to bDMARDs, may blunt isoprostane generation in the absence of significant effects on TxA2 biosynthesis, which could be associated with a higher frequency of non-melanoma skin cancer in patients long-term treated with anti-TNF-α agents [ 11 , 40 ]. In addition, MTX is found not to suppress TxA2 biosynthesis in whole blood from RA patients although MTX is a preferential COX-2 inhibitor [ 46 ].…”

Section: Adverse Effects Of Ra Treatment Drugs Are Related To the Coxmentioning

confidence: 99%

See 1 more Smart Citation

Can active components of licorice, glycyrrhizin and glycyrrhetinic acid, lick rheumatoid arthritis?

et al. 2015

View full text Add to dashboard Cite

OBJECTIVESThis review stated the possible application of the active components of licorice, glycyrrhizin (GL) and glycyrrhetinic acid (GA), in rheumatoid arthritis (RA) treatment based on the cyclooxygenase (COX)-2/thromboxane A2 (TxA2) pathway.METHODSThe extensive literature from inception to July 2015 was searched in PubMed central, and relevant reports were identified according to the purpose of this study.RESULTSThe active components of licorice GL and GA exert the potential anti-inflammatory effects through, at least in part, suppressing COX-2 and its downstream product TxA2. Additionally, the COX-2/TxA2 pathway, an auto-regulatory feedback loop, has been recently found to be a crucial mechanism underlying the pathogenesis of RA. However, TxA2 is neither the pharmacological target of non-steroidal anti-inflammatory drugs (NSAIDs) nor the target of disease modifying anti-rheumatic drugs (DMARDs), and the limitations and side effects of those drugs may be, at least in part, attributable to lack of the effects on the COX-2/TxA2 pathway. Therefore, GL and GA capable of targeting this pathway hold the potential as a novel add-on therapy in therapeutic strategy, which is supported by several bench experiments.CONCLUSIONSThe active components of licorice, GL and GA, could not only potentiate the therapeutic effects but also decrease the adverse effects of NSAIDs or DMARDs through suppressing the COX-2/TxA2 pathway during treatment course of RA.

show abstract

Section: Role Of the Cox-2/txa2 Pathway In The Pathogenesis Of Rasupporting

confidence: 86%

Section: Adverse Effects Of Ra Treatment Drugs Are Related To the Coxmentioning

confidence: 99%

Can active components of licorice, glycyrrhizin and glycyrrhetinic acid, lick rheumatoid arthritis?

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Ferrante and colleagues examined markers of oxidative stress and plasma levels of esRAGE in 54 subjects with RA and 20 healthy control subjects [65]. The authors reported that levels of urinary markers of oxidative stress were higher in RA patients vs .…”

Section: Age-rage and Oxidative Stress: Evidence From Human Subjectsmentioning

confidence: 99%

“…control subjects. In the latter case, esRAGE was the only independent predictor of the levels of urinary 11-dehydro-TXB2 [65]. The authors concluded that the anti-TNFα agents might only exert efficacy against isoprostane generation with no impact on thromboxane synthesis.…”

Section: Age-rage and Oxidative Stress: Evidence From Human Subjectsmentioning

confidence: 99%

Radical Roles for RAGE in the Pathogenesis of Oxidative Stress in Cardiovascular Diseases and Beyond

Daffu

Pozo

O’Shea

et al. 2013

IJMS

180

138

View full text Add to dashboard Cite

Oxidative stress is a central mechanism by which the receptor for advanced glycation endproducts (RAGE) mediates its pathological effects. Multiple experimental inquiries in RAGE-expressing cultured cells have demonstrated that ligand-RAGE interaction mediates generation of reactive oxygen species (ROS) and consequent downstream signal transduction and regulation of gene expression. The primary mechanism by which RAGE generates oxidative stress is via activation of NADPH oxidase; amplification mechanisms in the mitochondria may further drive ROS production. Recent studies indicating that the cytoplasmic domain of RAGE binds to the formin mDia1 provide further support for the critical roles of this pathway in oxidative stress; mDia1 was required for activation of rac1 and NADPH oxidase in primary murine aortic smooth muscle cells treated with RAGE ligand S100B. In vivo, in multiple distinct disease models in animals, RAGE action generates oxidative stress and modulates cellular/tissue fate in range of disorders, such as in myocardial ischemia, atherosclerosis, and aneurysm formation. Blockade or genetic deletion of RAGE was shown to be protective in these settings. Indeed, beyond cardiovascular disease, evidence is accruing in human subjects linking levels of RAGE ligands and soluble RAGE to oxidative stress in disorders such as doxorubicin toxicity, acetaminophen toxicity, neurodegeneration, hyperlipidemia, diabetes, preeclampsia, rheumatoid arthritis and pulmonary fibrosis. Blockade of RAGE signal transduction may be a key strategy for the prevention of the deleterious consequences of oxidative stress, particularly in chronic disease.

show abstract

“…Plasma esRAGE was measured using the B-Bridge ELISA (B-Bridge International, Cupertino, CA) as previously described [25]. This assay specifically measures the esRAGE/RAGEv1 protein only, due to the use of an antibody directed against the unique COOHterminal sequence of RAGE-v1 and does not cross-react with other potential forms of sRAGE.…”

Section: Measurementsmentioning

confidence: 99%

Decreased plasma endogenous soluble RAGE, and enhanced adipokine secretion, oxidative stress and platelet/coagulative activation identify non-alcoholic fatty liver disease among patients with familial combined hyperlipidemia and/or metabolic syndrome

Santilli

Blardi

Scapellato

et al. 2015

Vascular Pharmacology

Self Cite

View full text Add to dashboard Cite

Determinants of thromboxane biosynthesis in rheumatoid arthritis: Role of RAGE and oxidant stress

Cited by 19 publications

References 41 publications

Can active components of licorice, glycyrrhizin and glycyrrhetinic acid, lick rheumatoid arthritis?

Can active components of licorice, glycyrrhizin and glycyrrhetinic acid, lick rheumatoid arthritis?

Radical Roles for RAGE in the Pathogenesis of Oxidative Stress in Cardiovascular Diseases and Beyond

Decreased plasma endogenous soluble RAGE, and enhanced adipokine secretion, oxidative stress and platelet/coagulative activation identify non-alcoholic fatty liver disease among patients with familial combined hyperlipidemia and/or metabolic syndrome

Contact Info

Product

Resources

About