Monocyte stimulation by reactive oxygen species: Role of superoxide and intracellular Ca 2+

Volk, Thomas; Gerst, Jeffery W.; Faust-Belbe, G.; Stroehmann, Arne; Kox, Wolfgang J.

doi:10.1007/s000110050501

Cited by 32 publications

(19 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Importantly, ROS, via mechanisms not yet defined, release cytokines such as TNF␣ (31). This release has in turn been implicated in the pathogenesis of RA (32) based on the observation that anti-TNF␣ therapies suppress the development of CIA.…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin reduces the degree of arthritis caused by type II collagen in the mouse

Cuzzocrea

Mazzon

Paola

et al. 2005

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. Erythropoietin (EPO) is a potent stimulator of erythroid progenitor cells, and its expression is enhanced by hypoxia. The aim of this study was to investigate the effect of EPO on collagen-induced arthritis (CIA) in the mouse.Methods. CIA was induced by intradermal injection of bovine type II collagen (CII) and Freund's complete adjuvant. Starting on day 25, some of the mice with CIA received daily subcutaneous injections of EPO (1,000 units/kg). Two other groups of mice received sham treatment alone or sham treatment followed by EPO treatment, respectively. Arthritis was assessed clinically, radiologically, and histologically. Cytokine and chemokine levels were measured, and neutrophil infiltration into inflamed joints was quantitated. Immunohistochemistry studies were performed to measure protein nitrosylation. Chondrocyte apoptosis was assessed by TUNEL assay.Results. Macroscopic clinical evidence of CIA first appeared as periarticular erythema and edema in the hind paws. The incidence of CIA was 100% by day 27 in the CII-challenged mice, and the severity of CIA progressed over a 35-day period, with radiographic evaluation revealing focal resorption of bone. Histopathologic features of CIA included erosion of the cartilage at the joint margins. Treatment with EPO starting at the onset of arthritis (day 25) ameliorated the clinical signs on days 26-35 and improved histologic status in the joints and paws. The degree of oxidative and nitrosative damage was significantly reduced in EPO-treated mice as indicated by decreased nitrotyrosine formation and poly(ADP-ribose) polymerase activation. Plasma levels of the proinflammatory cytokine tumor necrosis factor ␣ were also significantly reduced by EPO treatment. In addition, EPO reduced the levels of apoptosis in chondrocytes in articular cartilage, as indicated by decreased TUNEL staining.Conclusion. These findings demonstrate that EPO exerts an antiinflammatory effect during chronic inflammation and is able to ameliorate the tissue damage associated with CIA.

show abstract

Section: Discussionmentioning

confidence: 99%

Erythropoietin reduces the degree of arthritis caused by type II collagen in the mouse

Cuzzocrea

Mazzon

Paola

et al. 2005

Arthritis & Rheumatism

View full text Add to dashboard Cite

show abstract

“…Reactive oxygen species play an important role in the activation of monocytes to increase TNF-␣ production, thus contributing to the development of ischemia/reperfusion-induced tissue injury (Volk et al, 1999). AP-1 has been shown to be implicated in the ischemia/ reperfusion-induced increase of TNF-␣ production (Yeh et al, 2000), and inhibition of AP-1 activation by gabexate mesilate might explain the therapeutic effect in the tissue injury induced by ischemia/reperfusion.…”

Section: Inhibition Of Tnf-␣ Production By Gabexate Mesilate In Vitromentioning

confidence: 99%

Gabexate Mesilate, a Synthetic Protease Inhibitor, Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor-α Production by Inhibiting Activation of Both Nuclear Factor-κB and Activator Protein-1 in Human Monocytes

Yüksel¹,

Okajima²,

Uchiba³

et al. 2003

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Gabexate mesilate, a synthetic protease inhibitor, was shown to be effective in treating patients with sepsis-associated disseminated intravascular coagulation in which tumor necrosis factor-␣ (TNF-␣) plays a critical role. We demonstrated that gabexate mesilate reduced lipopolysaccharide (LPS)-induced tissue injury by inhibiting TNF-␣ production in rats. In the present study, we analyzed the mechanism(s) by which gabexate mesilate inhibits LPS-induced TNF-␣ production in human monocytes in vitro. Gabexate mesilate inhibited the production of TNF-␣ in monocytes stimulated with LPS. Gabexate mesilate inhibited both the binding of nuclear factor-B (NF-B) to target sites and the degradation of inhibitory B␣. Gabexate mesilate also inhibited both the binding of activator protein-1 (AP-1) to target sites and the activation of mitogen-activated protein kinase pathways. These observations strongly suggest that gabexate mesilate inhibited LPS-induced TNF-␣ production in human monocytes by inhibiting activation of both NF-B and AP-1. Inhibition of TNF-␣ production by gabexate mesilate might explain at least partly its therapeutic effects in animals given LPS and those in patients with sepsis.

show abstract

“…These enzymes include the manganese enzyme in mitochondria, SOD2, and copper͞zinc enzymes present in the cytosol, SOD1, or extracellular surfaces, SOD3. The importance of SOD2 is highlighted by the findings that, in contrast to SOD1 (18) and SOD3 (19), SOD2 knockout is lethal to mice (20)(21)(22) (26,27), recruitment of neutrophils at sites of inflammation (28,29), lipid peroxidation and oxidation, DNA single strand damage (30), release of cytokines such as TNF-␣ and IL-1␤ (31,32), and formation of ONOO Ϫ , a potent cytotoxic and proinflammatory molecule (33)(34)(35)(36)(37). One of the most important features of shock that ultimately determines survival is the reversibility of inadequate organ perfusion secondary to loss of vasomotor tone, which in turn leads to reduced venous return, reduced cardiac output, and severe arterial hypotension (5).…”

mentioning

confidence: 99%

Inactivation of catecholamines by superoxide gives new insights on the pathogenesis of septic shock

Macarthur

Westfall

Riley

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

191

129

View full text Add to dashboard Cite

Monocyte stimulation by reactive oxygen species: Role of superoxide and intracellular Ca 2+

Abstract: We propose that superoxide activates human mononuclear cells in a Ca2+-dependent manner.

Cited by 32 publications

References 14 publications

Erythropoietin reduces the degree of arthritis caused by type II collagen in the mouse

Erythropoietin reduces the degree of arthritis caused by type II collagen in the mouse

Gabexate Mesilate, a Synthetic Protease Inhibitor, Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor-α Production by Inhibiting Activation of Both Nuclear Factor-κB and Activator Protein-1 in Human Monocytes

Inactivation of catecholamines by superoxide gives new insights on the pathogenesis of septic shock

Contact Info

Product

Resources

About