Nuclear Heat Shock Protein 72 as a Negative Regulator of Oxidative Stress (Hydrogen Peroxide)-Induced HMGB1 Cytoplasmic Translocation and Release

Tang, Daolin; Kang, Rui; Xiao, Weimin; Jiang, Lei; Liu, Meidong; Shi, Yanhong; Wang, Kangkai; Wang, Haichao; Xiao, Xianzhong

doi:10.4049/jimmunol.178.11.7376

Cited by 90 publications

(82 citation statements)

References 56 publications

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“…17,18 In all, 30 mg of protein per lane was run on a denaturing 10% SDSpolyacrylamide gel and subsequently transferred to polyvinylidene fluoride membranes via semidry transfer. After blocking the membrane at room temperature for 3 h, the membrane was incubated overnight at 4 1C with various primary antibodies.…”

Section: Western Blotting Analysismentioning

confidence: 99%

“…Before immunoprecipitation, samples containing equal amounts of proteins were pre-cleared with Protein A or protein G agarose/sepharose (Millipore) (4 1C, 3 h) and subsequently incubated with various irrelevant immunoglobulin-G or specific antibodies (5 mg/ml) in the presence of protein A or G agarose/sepharose beads for 2 h or overnight at 4 1C while gently shaking. 16,17,19 Following incubation, agarose/ sepharose beads were washed extensively with phosphatebuffered saline and proteins eluted by boiling in 2 Â SDS sample buffer before SDS-polyacrylamide gel electrophoresis.…”

Section: Immunoprecipitation Analysismentioning

confidence: 99%

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HMGB1-induced autophagy promotes chemotherapy resistance in leukemia cells

et al. 2010

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Autophagy, a tightly regulated lysosome-dependent catabolic pathway, is important in the regulation of cancer development and progression and in determining the response of tumor cells to anticancer therapy. However, the role of autophagy in leukemia still remains largely unknown. Here we show that high-mobility group box 1 (HMGB1), the best characterized damage-associated molecular pattern, was released from leukemia cell lines after chemotherapy-induced cytotoxicity and activated autophagy to protect against injury. Treatment with HMGB1-neutralizing antibodies increased the sensitivity of leukemia cells to chemotherapy; whereas, exogenous HMGB1 rendered these cells more resistant to drug-induced cytotoxicity. Moreover, exogenous HMGB1 increased autophagy as evaluated by increased expression of the autophagic marker microtubule-associated protein light chain 3-II, degradation of sequestosome 1 (p62) and autophagosome formation. Furthermore, knockdown or pharmacological inhibition of either phosphoinositide 3-kinase-III or extracellular signal-regulated kinase kinase mitogen-activated protein kinase kinase/extracellular signal-regulated protein kinase inhibited HMGB1-induced autophagy. Taken together, these results suggest that HMGB1 release after chemotherapy is a critical regulator of autophagy and a potential drug target for therapeutic interventions in leukemia.

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Section: Western Blotting Analysismentioning

confidence: 99%

Section: Immunoprecipitation Analysismentioning

confidence: 99%

HMGB1-induced autophagy promotes chemotherapy resistance in leukemia cells

et al. 2010

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“…Proteins in cell lysates were resolved on 4%-12% Criterion XT Bis-Tris gels (Bio-Rad, Hercules, CA) and transferred to a nitrocellulose membrane as previously described (42,43). After blocking, the membrane was incubated for 2 h at 25°C or overnight at 4°C with various primary antibodies.…”

Section: Western Blot Analysismentioning

confidence: 99%

The Receptor for Advanced Glycation End-Products (RAGE) Protects Pancreatic Tumor Cells Against Oxidative Injury

Kang

Tang

Livesey

et al. 2011

Antioxidants & Redox Signaling

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Reactive oxygen species, including hydrogen peroxide (H 2 O 2 ), can cause toxicity and act as signaling molecules in various pathways regulating both cell survival and cell death. However, the sequence of events between the oxidative insult and cell damage remains unclear. In the current study, we investigated the effect of oxidative stress on activation of the Receptor for Advanced Glycation End-products (RAGE) and subsequent protection against H 2 O 2 -induced pancreatic tumor cell damage. We found that exposure of pancreatic tumor cells to H 2 O 2 provoked a nuclear factor kappa B (NF-kB)-dependent increase in RAGE expression. Further, suppression of RAGE expression by RNA interference increased the sensitivity of pancreatic tumor cells to oxidative injury. Furthermore, targeted knockdown of RAGE led to increased cell death by apoptosis and diminished cell survival by autophagy during H 2 O 2 -induced oxidative injury. Moreover, we demonstrate that RAGE is a positive feedback regulator for NF-kB as knockdown of RAGE decreased H 2 O 2 -induced activity of NF-kB. Taken together, these results suggest that RAGE is an important regulator of oxidative injury. Antioxid. Redox Signal. 15, 2175-2184.

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“…Hitherto, studies have shown that JNK inhibition and an increase in the expression of HSP72 suppress HMGB1 release by LPS-stimulated RAW264.7 cells (16,17). Contrary to these reports, both Ume extract and authentic OA failed to affect JNK activation, induction of HSP72 protein, or anticoagulant activity (data not presented).…”

Section: Discussionmentioning

confidence: 61%

“…Similarly, a blockade of HMGB1 activity by administering thrombomodulin, an anti-coagulant protein, to rodents along with thrombin ameliorated the clinical and histological features of the disease (6,7,11), and the inhibition of HMGB1 release was found to be protective against experimental sepsis (2). Several other substances, including the N-terminal kinase activation (JNK) inhibitors and heat shock protein (HSP) 72, are known to inhibit HMGB1 release from lipopolysaccharide (LPS)-stimulated macrophages (13)(14)(15)(16)(17)(18)(19)(20)(21)(22). Additionally, natural substances, such as green tea and deep ocean water (DOW), have been shown to inhibit HMGB1 release in RAW264.7 cells (23,24).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of HMGB1 release inhibition from RAW264.7 cells by oleanolic acid in Prunus mume Sieb. et Zucc.

Kikuchi

Hashiguchi²,

Masuda³

et al. 2009

Int J Mol Med

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Abstract. High mobility group box-1 protein (HMGB1), primarily from the nucleus, is released into the extracellular milieu either passively from necrotic cells or actively through secretion by monocytes/macrophages. Extracellular HMGB1 acts as a potent inflammatory agent by promoting the release of cytokines such as tumor necrosis factor (TNF)-·, has procoagulant activity, and is involved in death due to sepsis. Accordingly, HMGB1 is an appropriate therapeutic target. In this study, we found that an extract of Prunus mume Sieb. et Zucc. (Ume) fruit (Ume extract), an abundant source of triterpenoids, strongly inhibited HMGB1 release from lipopolysaccharide (LPS)-stimulated macrophage-like RAW264.7 cells. The inhibitory effect on HMGB1 release was enhanced by authentic oleanolic acid (OA), a naturally occurring triterpenoid. Similarly, the HMGB1 release inhibitor in Ume extract was found to be OA. Regarding the mechanisms of the inhibition of HMGB1 release, the OA or Ume extract was found to activate the transcription factor Nrf2, which binds to the antioxidative responsive element, and subsequently the heme oxygenase (HO)-1 protein was induced, indicating that the inhibition of HMGB1 release from LPS-stimulated RAW264.7 cells was mediated via the Nrf2/HO-1 system; an essentially antioxidant effect. These results suggested that natural sources of triterpenoids warrant further evaluation as 'rescue' therapeutics for sepsis and other potentially fatal systemic inflammatory disorders.

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Nuclear Heat Shock Protein 72 as a Negative Regulator of Oxidative Stress (Hydrogen Peroxide)-Induced HMGB1 Cytoplasmic Translocation and Release

Cited by 90 publications

References 56 publications

HMGB1-induced autophagy promotes chemotherapy resistance in leukemia cells

HMGB1-induced autophagy promotes chemotherapy resistance in leukemia cells

The Receptor for Advanced Glycation End-Products (RAGE) Protects Pancreatic Tumor Cells Against Oxidative Injury

Mechanism of HMGB1 release inhibition from RAW264.7 cells by oleanolic acid in Prunus mume Sieb. et Zucc.

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