Diphenyleneiodonium inhibits NF‐κB activation and iNOS expression induced by IL‐1β: involvement of reactive oxygen species

Mendes, Alexandrina Ferreira; Carvalho, AP; Caramona, Maria Margarida; Lopes, María Celeste

doi:10.1080/09629350120080401

Cited by 39 publications

(43 citation statements)

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“…The activation of p38 MAP kinase and NF-κB nuclear translocation by HA oligos are in common with the stimulation of NO due to treatment of cells with IL-1 (Badger et al, 1998;Clancy et al, 2004;Mendes et al, 2001). In this study we demonstrated that this similarity was not due to HA oligos -induced autocrine release of endogenous IL-1 (Fig.…”

Section: Discussionsupporting

confidence: 61%

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Hyaluronan fragments activate nitric oxide synthase and the production of nitric oxide by articular chondrocytes

Iacob

Knudson

2006

The International Journal of Biochemistry & Cell Biology

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Chondrocyte CD44 receptors anchor hyaluronan to the cell surface, enabling the assembly and retention of proteoglycan aggregates in the pericellular matrix. Hyaluronan-CD44 interactions also provide signaling important for maintaining cartilage homeostasis. Disruption of chondrocyte-hyaluronan contact alters CD44 occupancy, initiating alternative signaling cascades. Treatment with hyaluronan oligosaccharides is one approach to uncouple CD44 receptors from its native ligand, hyaluronan. In bovine articular chondrocytes, treatment with hyaluronan oligosaccharides or purified hyaluronan hexasaccharides induced the production of nitric oxide that mirrored nitric oxide production following interleukin-1 treatment. In contrast, 120 and 1260 kDa hyaluronan did not induce production of nitric oxide. Human chondrocytes responded similarly to treatment with hyaluronan or hyaluronan oligosaccharides. Nitric oxide production from chondrocytes was mediated by activation of the inducible nitric oxide synthase, as confirmed by mRNA expression and inhibition of nitric oxide production by diphenyleneiodonium. Cotreatment of chondrocytes with hyaluronan oligosaccharides and interleukin-1 did not demonstrate additive effects. Blocking interleukin-1 receptors with an antagonist did not abolish the production of nitric oxide induced by treatment with hyaluronan oligosaccharides. Moreover, only COS-7 following transfection with a pCD44, not the CD44-null parental cells, responded to treatment with hyaluronan oligosaccharides by releasing nitric oxide. This study demonstrates a novel signaling potential by hyaluronan fragments, in lieu of endogenous hyaluronan-chondrocyte interactions, resulting in the activation of inducible nitric oxide synthase.

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Section: Discussionsupporting

confidence: 61%

“…To further explore the role of the iNOS in the NO signaling pathway, bovine chondrocytes in alginate beads were stimulated with IL-1α or HA oligos in the presence or absence of DPI, a flavin-dependent inhibitor of iNOS enzymatic activity (Mendes, Carvalho, Caramona, & Lopes, 2001). As shown in Fig.…”

Section: Induction Of Inosmentioning

confidence: 99%

Hyaluronan fragments activate nitric oxide synthase and the production of nitric oxide by articular chondrocytes

Iacob

Knudson

2006

The International Journal of Biochemistry & Cell Biology

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“…EGF, a known stimulant of Nox1, was found to induce chemiluminescence in BeWo cells and its effect was inhibited by DPI. Although DPI was found to inhibit all FAD-binding enzymes, including nitric oxide synthase [38] and P450 enzymes [39] at higher concentrations, a relatively lower concentration (e.g., 30 μM, not shown) needed for EGF-induced activation suggests that an NADPH oxidase was involved. Previous studies employing Western blot analysis has shown multiple bands of Nox1 in vascular smooth muscle cells [40] and in Cos-7 cells transfected with Nox1 expression plasmid [41].…”

Section: Discussionmentioning

confidence: 99%

Expression of NADPH Oxidase Isoform 1 (Nox1) in Human Placenta: Involvement in Preeclampsia

et al. 2006

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Increased oxidative stress in the placenta has been associated with preeclampsia (PE), a clinical syndrome involving placental pathology. The enzymatic sources of reactive oxygen species in the human placenta are as yet unidentified. We hypothesized that NADPH oxidase is a main source of reactive oxygen species in the placenta and its expression may change in PE. Employing RTPCR, we have amplified a novel NADPH oxidase isoform Nox1 from human choriocarcinoma BeWo cells. Using polyclonal anti-peptide antiserum recognizing unique Nox1 peptide sequences, we identified by immunohistochemistry and cell fractionation that Nox1 protein localizes in the BeWo cell membrane structures. Immunohistochemistry of normal placental tissues showed that Nox1 was localized in syncytiotrophoblasts, in villous vascular endothelium, and in some stromal cells. At the immunohistochemical level Nox1 expression was significantly increased in syncytiotrophoblast and endothelial cells in placentas from patients with preeclampsia as compared to gestational agematched controls. Western blot analysis of whole placental homogenate confirmed this increase. Our data suggests that increased Nox1 expression is associated with the increased oxidative stress found in these placentas.

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“…Spermine, an end-product of polyamine biosynthesis from L-arginine, is a competitive inhibitor of n-and i-NOS [23][24][25]. DPI is an i-NOS inhibitor [26,27]. All drugs were prepared as stock solutions in distilled water.…”

Section: Methodsmentioning

confidence: 99%

The Effect of e-, i-, and n-Nitric Oxide Synthase Inhibition on Colonic Motility in Normal and Muscular Dystrophy (Mdx) Mice

Tameyasu

Ogura

Ogihara

2004

JJP

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(5 µM) reduced the magnitude of local, rhythmic contractions (LC) paced by the interstitial cells of Cajal (ICC), but 1,3-PBIT (50 µM) increased their magnitude. There was no difference in the effect of spermine and 1,3-PBIT on the LC between mdx and control colon. The results suggest an inhibition of MMC by high concentrations of e-, i-, and n-NOS inhibitors, modulation of ICC activity by e-NOS, and greater susceptibility of MMC to n-NOS inhibition in the mdx proximal than in the control colon, which is very likely because of a deficit in n-NOS in the mdx smooth muscle affecting the MMC pacemaker. A deficit in the effect of mdx smooth muscle n-NOS on an MMC pacemaker may be the origin of diarrhea or constipation in human DMD. Japanese Journal of Physiology Vol. 54, [555][556][557][558][559][560][561][562][563][564][565][566] 2004 Abstract: To explore the origin of diarrhea or constipation in human Duchenne muscular dystrophy (DMD), the effect of the inhibition of e-, i-, and n-nitric oxide synthase (NOS) on the motility of proximal and distal segments of colon of muscular dystrophy (mdx) and control mice was studied. The frequency of migrating motor complexes (MMC) was higher in the proximal than in the distal segments in mdx colon (0.56 vs. 0.25 cpm) and in the control colon (0.7 vs. 0.25 cpm), and there was no difference when mdx was compared to control segments. High concentrations of NOS inhibitors, including 1,3-PBIT dihydrobromide (1,3-PBIT) and spermine, inhibited MMC. The dose of spermine required to inhibit MMC was lower for the proximal mdx colon than for the distal mdx or control colon. In the presence of tetrodotoxin, spermine (1 mM) and 1,3-PBIT

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Diphenyleneiodonium inhibits NF‐κB activation and iNOS expression induced by IL‐1β: involvement of reactive oxygen species

Cited by 39 publications

References 43 publications

Hyaluronan fragments activate nitric oxide synthase and the production of nitric oxide by articular chondrocytes

Hyaluronan fragments activate nitric oxide synthase and the production of nitric oxide by articular chondrocytes

Expression of NADPH Oxidase Isoform 1 (Nox1) in Human Placenta: Involvement in Preeclampsia

The Effect of e-, i-, and n-Nitric Oxide Synthase Inhibition on Colonic Motility in Normal and Muscular Dystrophy (Mdx) Mice

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