Prevention of TNF-induced necrotic cell death by rottlerin through a Nox1 NADPH oxidase

Byun, Hee Sun; Won, Minho; Park, Kyeong Ah; Kim, Young‐Rae; Choi, Byung Lyul; Lee, Hyunji; Hong, Jang Hee; Li, Piao; Park, Jongsun; Kim, Jin Man; Kweon, Gi Ryang; Kang, Sung Hyun; Han, Jin; Hur, Gang Min

doi:10.3858/emm.2008.40.2.186

Cited by 21 publications

(13 citation statements)

References 29 publications

(35 reference statements)

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“…Slug suppression by RNA interference markedly enhanced H 2 O 2 -induced apoptosis in RA FLS, and this was mediated by increased caspase-3 activation. H 2 O 2 -induced cell necrosis could also have contributed to FLS death in our experiment (Byun et al, 2008), but obvious influence of Slug suppression on FLS apoptosis has been demonstrated by apoptosis specific ELISA and caspase-3 activation assay. Because experiments comparing RA FLS with osteoarthritis FLS were not performed, we don't know whether these results are specific to RA FLS and it is unclear whether these Slug mediated apoptotic regulation is also operating in osteoarthritis or normal FLS.…”

Section: Discussionmentioning

confidence: 62%

Slug suppression induces apoptosis via Puma transactivation in rheumatoid arthritis fibroblast-like synoviocytes treated with hydrogen peroxide

et al. 2010

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Inadequate apoptosis contributes to synovial hyperplasia in rheumatoid arthritis (RA). Recent study shows that low expression of Puma might be partially responsible for the decreased apoptosis of fibroblast-like synoviocytes (FLS). Slug, a highly conserved zinc finger transcriptional repressor, is known to antagonize apoptosis of hematopoietic progenitor cells by repressing Puma transactivation. In this study, we examined the expression and function of Slug in RA FLS.

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Section: Discussionmentioning

confidence: 62%

Slug suppression induces apoptosis via Puma transactivation in rheumatoid arthritis fibroblast-like synoviocytes treated with hydrogen peroxide

et al. 2010

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“…TNF-TNFR complex has also been shown to enhance NADPH oxidase activity promoting a burst of oxidative stress and leading to necrotic cell death (141,142).…”

Section: Cross-linking Of Tnf and Tnfr Type I Dependent Pathwaymentioning

confidence: 99%

Cell Death Mechanisms Induced by Cytotoxic Lymphocytes

et al. 2009

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One of the functions of the immune system is to recognize and destroy abnormal or infected cells to maintain homeostasis. This is accomplished by cytotoxic lymphocytes. Cytotoxicity is a highly organized multifactor process. Here, we reviewed the apoptosis pathways induced by the two main cytotoxic lymphocyte subsets, natural killer (NK) cells and CD8 + T cells. In base to recent experimental evidence, we reviewed NK receptors involved in recognition of target-cell, as well as lytic molecules such as perforin, granzymes-A and -B, and granulysin. In addition, we reviewed the Fas-FasL intercellular linkage mediated pathway, and briefly the cross-linking of tumor necrosis factor (TNF) and TNF receptor pathway. We discussed three models of possible molecular interaction between lytic molecules from effector cytotoxic cells and target-cell membrane to induction of apoptosis. Cellular & Molecular Immunology. 2009;6(1):15-25.

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“…DN-p38 MAPK mutant construct was kindly provided by Dr Surh (Seoul National University, Seoul, Korea) . DN-PKCd adenovirus was provided by Dr Hur (Chungnam National University, Daejeon, Korea) (Byun et al, 2008). Cells were transfected according to the manufacturer's instructions with Lipofectamine 2000 transfection reagent obtained from Invitrogen (Carlsbad, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Lysophosphatidic acid augments human hepatocellular carcinoma cell invasion through LPA1 receptor and MMP-9 expression

et al. 2010

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Lysophosphatidic acid (LPA), produced extracellularly by autotaxin (ATX), has diverse biological activities implicated in tumor initiation and progression, including increasing cell survival, angiogenesis, invasion and metastasis. ATX, LPA and the matrix metalloproteinase (MMP)-9 have all been implicated in hepatocellular carcinoma (HCC) invasion and metastasis. We, thus sought to determine whether ATX with subsequent LPA production and action, including induction of MMP-9 could provide a unifying mechanism. ATX transcripts and LPA receptor type 1 (LPA1) protein are elevated in HCC compared with normal tissues. Silencing or pharmacological inhibition of LPA1 significantly attenuated LPA-induced MMP-9 expression and HCC cell invasion. Further, reducing MMP-9 activity or expression significantly inhibits LPA-induced HCC cell invasion, demonstrating that MMP-9 is downstream of LPA1. Inhibition of phosphoinositide-3 kinase (PI3K) signaling or dominantnegative mutants of protein kinase Cd and p38 mitogenactivated protein kinase (MAPK) abrogated LPA-induced MMP-9 expression and subsequent invasion. We thus demonstrate a mechanistic cascade of ATX-producing LPA with LPA activating LPA1 and inducing MMP-9 through coordinate activation of the PI3K and the p38 MPAK signaling cascades, providing novel biomarkers and potential therapeutic targets for HCC.

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Prevention of TNF-induced necrotic cell death by rottlerin through a Nox1 NADPH oxidase

Cited by 21 publications

References 29 publications

Slug suppression induces apoptosis via Puma transactivation in rheumatoid arthritis fibroblast-like synoviocytes treated with hydrogen peroxide

Slug suppression induces apoptosis via Puma transactivation in rheumatoid arthritis fibroblast-like synoviocytes treated with hydrogen peroxide

Cell Death Mechanisms Induced by Cytotoxic Lymphocytes

Lysophosphatidic acid augments human hepatocellular carcinoma cell invasion through LPA1 receptor and MMP-9 expression

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