Cell type-specific role for reactive oxygen species in nuclear factor-kappaB activation by Interleukin-1

Bonizzi, Giuseppina; Piette, Jacques; Merville, Marie Paule; Bours, Vincent

doi:10.1016/s0006-2952(99)00290-7

Cited by 146 publications

(88 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…NF-B was one of the first transcription factors shown to be activated by ROS (5). Although ROS were initially proposed to be central mediators of NF-B activation (7), this role depends both on cell type and on cell status (11,(52)(53)(54)(55). In some cell types, NF-B activity is actually inhibited by exposure to H 2 O 2 (54).…”

Section: Discussionmentioning

confidence: 99%

Roles of TRP14, a Thioredoxin-related Protein in Tumor Necrosis Factor-α Signaling Pathways

Jeong

Chang

Boja

et al. 2004

Journal of Biological Chemistry

View full text Add to dashboard Cite

The possible roles of a 14-kDa human thioredoxin (Trx)-related protein (TRP14) in TNF-␣ signaling were studied in comparison with those of Trx1 by RNA interference in HeLa cells. Depletion of TRP14 augmented the TNF-␣-induced phosphorylation and degradation of I B␣ as well as the consequent activation of NF-B to a greater extent than did Trx1 depletion. Deficiency of TRP14 or Trx1 enhanced TNF-␣-induced activation of caspases and subsequent apoptosis by a similar extent. The TNF-␣-induced activation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (MAPKs), however, was promoted by depletion of TRP14 but not by that of Trx1. Unlike Trx1, TRP14 neither associated with nor inhibited the kinase activity of apoptosis signal-regulating kinase-1 (ASK1), an upstream activator of JNK and p38. In combination with the results in the accompanying paper that TRP14 did not reduce the known substrates of Trx1, these results suggest that TRP14 modulates TNF-␣ signaling pathways, provably by interacting with proteins distinct from the targets of Trx1. In an effort to identify target proteins of TRP14, a mutant of TRP14, in which the active site cysteine (Cys 46 ) was substituted with serine, was shown to form a disulfide-linked complex with LC8 cytoplasmic dynein light chain. The complex was detected in HeLa cells treated with H 2 O 2 or TNF-␣ but not in untreated cells, suggesting that LC8 cytoplasmic dynein light chain is a possible substrate of TRP14.The cellular redox state is affected not only by normal respiration and metabolism but also by the transient production of reactive oxygen species (ROS) 1 that results from the ligation of various cell surface receptors (1-3). Tumor necrosis factor-␣ (TNF-␣) was one of the first receptor ligands shown to generate ROS in nonphagocytic cells and is among the ligands whose signaling pathways have been studied most in relation to ROS production (4, 5). The binding of TNF-␣ to TNF receptor 1 (TNFR1) generates both proapoptotic and prosurvival signals by inducing the formation of a multiprotein signaling complex at the cell membrane. This complex in turn triggers the caspase cascade, the activation of specific kinases such as the I B kinase (IKK) complex and mitogen-activated protein kinases (MAPKs), and the transcription of various genes mediated by nuclear factor-B (NF-B) and activator protein-1 (AP-1) (6 -10). Many TNF-␣ signaling pathways are activated by ROS (7, 11-16) and attenuated by Trx overexpression (17-25).In the accompanying study (26), we identified and characterized a 14-kDa cytosolic protein, designated Trx-related protein 14 (TRP14). Here we studied the possible roles of TRP14 in TNF-␣ signaling in comparison with those of Trx1 by RNA interference (RNAi) in HeLa cells. Partial depletion of TRP14 or Trx1 by RNAi resulted in enhancement of TNF-␣-induced activation of caspases and NF-B. The TNF-␣-induced activation of c-Jun-N-terminal kinase (JNK) and p38 MAPK, however, was augmented by depletion of TRP14 but not by that of Trx1. Furthermore, unl...

show abstract

Section: Discussionmentioning

confidence: 99%

Roles of TRP14, a Thioredoxin-related Protein in Tumor Necrosis Factor-α Signaling Pathways

Jeong

Chang

Boja

et al. 2004

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Distinct signal transduction pathways can mediate NFkB induction in different cell types (Bonizzi et al, 1997;Ghosh and Karin, 2002), so we investigated whether zerumbone could block TNF-induced NF-kB activation in human myeloid leukemia KBM-5 ( Figure 4a) and human embryonic kidney A293 (Figure 4b). TNF activated NF-kB in both cell types, and zerumbone completely inhibited the activation (Figure 4a, b).…”

Section: Zerumbone Suppresses Tnf-induced Invasion Activitymentioning

confidence: 99%

Zerumbone abolishes NF-κB and IκBα kinase activation leading to suppression of antiapoptotic and metastatic gene expression, upregulation of apoptosis, and downregulation of invasion

2005

View full text Add to dashboard Cite

“…Proinflammatory cytokines and chemokines, which are implicated in the progression of arthritis, have been demonstrated to induce the production of ROS in a variety of cells (28)(29)(30)(31). In addition, it has been reported that receptor-mediated ROS generation is an upstream event in the activation of the MAPKs phosphatidylinositol 3-kinase and NF-B (28,31,32).…”

mentioning

confidence: 99%

Water‐soluble C60 fullerene prevents degeneration of articular cartilage in osteoarthritis via down‐regulation of chondrocyte catabolic activity and inhibition of cartilage degeneration during disease development

Yudoh

Shishido

Murayama

et al. 2007

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. Studies have shown the roles of oxidative stress in the pathogenesis of osteoarthritis (OA) and induction of chondrocyte senescence during OA progression. The aim of this study was to examine the potential of a strong free-radical scavenger, watersoluble fullerene (C60), as a protective agent against catabolic stress-induced degeneration of articular cartilage in OA, both in vitro and in vivo.Methods. In the presence or absence of C60 (100 M), human chondrocytes were incubated with interleukin-1␤ (10 ng/ml) or H 2 O 2 (100 M), and chondrocyte activity was analyzed. An animal model of OA was produced in rabbits by resection of the medial meniscus and medial collateral ligament. Rabbits were divided into 5 subgroups: sham operation or treatment with C60 at 0.1 M, 1 M, 10 M, or 40 M. The left knee joint was injected intraarticularly with watersoluble C60 (2 ml), while, as a control, the right knee joint received 50% polyethylene glycol (2 ml), once weekly for 4 weeks or 8 weeks. Knee bone and cartilage tissue were prepared for histologic analysis. In addition, in the OA rabbit model, the effect of C60 (10 M) on degeneration of articular cartilage was compared with that of sodium hyaluronate (HA) (5 mg/ml).Results. C60 (100 M) inhibited the catabolic stress-induced production of matrix-degrading enzymes (matrix metalloproteinases 1, 3, and 13), downregulation of matrix production, and apoptosis and premature senescence in human chondrocytes in vitro.In rabbits with OA, treatment with water-soluble C60 significantly reduced articular cartilage degeneration, whereas control knee joints showed progression of cartilage degeneration with time. This inhibitory effect was dose dependent, and was superior to that of HA. Combined treatment with C60 and HA yielded a significant reduction in cartilage degeneration compared with either treatment alone. Conclusion.The results indicate that C60 fullerene is a potential therapeutic agent for the protection of articular cartilage against progression of OA.During the development of osteoarthritis (OA), mechanical and chemical stresses on articular cartilage change the stable cellular activities of chondrocytes and stimulate the production of growth factors and matrix proteins as well as inflammation mediators (1-4). It is well known that catabolic-stressed chondrocytes produce excess amounts of reactive oxygen species (ROS) (superoxide, nitric oxide, hydrogen peroxide, and peroxynitrite) as well as proinflammatory cytokines and chemokines (4-9).Studies have provided ample confirmation of the generation of ROS and the depletion of cellular antioxidants in degenerated articular cartilage (8-10). Numerous reports have indicated that the degeneration of articular cartilage is partially mediated by oxygenderived free radicals (8-12). Kurz et al reported that the extent of mechanical stress on articular cartilage is sufficient to stimulate an excess production of ROS from chondrocytes, leading to depolymerization of hyaluronic acid and chondrocyte death (11,12). Similarly, Gree...

show abstract

Cell type-specific role for reactive oxygen species in nuclear factor-kappaB activation by Interleukin-1

Cited by 146 publications

References 39 publications

Roles of TRP14, a Thioredoxin-related Protein in Tumor Necrosis Factor-α Signaling Pathways

Roles of TRP14, a Thioredoxin-related Protein in Tumor Necrosis Factor-α Signaling Pathways

Zerumbone abolishes NF-κB and IκBα kinase activation leading to suppression of antiapoptotic and metastatic gene expression, upregulation of apoptosis, and downregulation of invasion

Water‐soluble C60 fullerene prevents degeneration of articular cartilage in osteoarthritis via down‐regulation of chondrocyte catabolic activity and inhibition of cartilage degeneration during disease development

Contact Info

Product

Resources

About