High-Mobility Group Box 1 Contributes to Lethality of Endotoxemia in Heme Oxygenase-1–Deficient Mice

Takamiya, Rina; Hung, Chi Chih; Hall, Sean; Fukunaga, Koichi; Nagaishi, Takashi; Maeno, Toshitaka; Owen, Caroline A.; Macias, Alvaro A.; Fredenburgh, Laura E.; Ishizaka, Akitoshi; Blumberg, Richard S.; Baron, Rebecca M.; Perrella, Mark A.

doi:10.1165/rcmb.2008-0331oc

Cited by 65 publications

(44 citation statements)

References 48 publications

(56 reference statements)

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“…Moreover, delayed administration of CORM-2 (12 h after LPS or CLP) significantly inhibited HMGB1 levels without alterations in serum levels of TNF-␣ or IL-1␤, suggesting that inhibition of HMGB1 is a clue for HO-1 and/or COmediated improved survival. Consistent with a recent report that CORM-2 was able to suppress the increased circulating HMGB1 in HO-1(Ϫ/Ϫ) mice and rescued HO-1(Ϫ/Ϫ) mice from the lethality of endotoxemia (Takamiya et al, 2008), the finding of reduced serum levels of HMGB1 by CO and/or HO-1 inducers implies that CO is important regulator of HMGB1 release. However, they (Takamiya et al, 2008) Fig.…”

Section: Co Inhibits Hmgb1 Release In Lps-and Clp-induced Sepsis 179supporting

confidence: 90%

“…Consistent with a recent report that CORM-2 was able to suppress the increased circulating HMGB1 in HO-1(Ϫ/Ϫ) mice and rescued HO-1(Ϫ/Ϫ) mice from the lethality of endotoxemia (Takamiya et al, 2008), the finding of reduced serum levels of HMGB1 by CO and/or HO-1 inducers implies that CO is important regulator of HMGB1 release. However, they (Takamiya et al, 2008) Fig. 10.…”

Section: Co Inhibits Hmgb1 Release In Lps-and Clp-induced Sepsis 179supporting

confidence: 90%

“…Very recently, Takamiya et al (2008) reported that elevated circulating levels of HMGB1 contributed to LPS-induced mortality in the absence of HO-1 rodents, which further reinforces our hypothesis.…”

Section: Interleukin (Il)-1␤ Interferon-␤ and N -Nitro-l-arginine Msupporting

confidence: 88%

“…Although HMGB1 was first implicated as an important endogenous signaling molecule (Wang et al, 1999) and as a late mediator of endotoxin related lethality in mice, the relationship between inhibition of HMGB1 release and HO-1 up-regulation has recently been reported in LPS-induced acute lung injury (Gong et al, 2008). The relationship between HO-1 and HMGB1 in an experimental model of sepsis and septic shock has also been reported (Takamiya et al, 2008). These authors reported that circulating levels of HMGB1 were higher in HO-1(Ϫ/Ϫ) mice when treated with a low dose of LPS (5 mg/kg), a dose in which wild-type mice do not exhibit increased circulating …”

Section: Discussionmentioning

confidence: 99%

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Heme-Oxygenase-1 Induction and Carbon Monoxide-Releasing Molecule Inhibit Lipopolysaccharide (LPS)-Induced High-Mobility Group Box 1 Release in Vitro and Improve Survival of Mice in LPS- and Cecal Ligation and Puncture-Induced Sepsis Model in Vivo

Tsoyi

Lee²,

Lee³

et al. 2009

Mol Pharmacol

180

110

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We examined our hypothesis that heme-oxygenase-1 (HO-1)-derived carbon monoxide (CO) inhibits the release of highmobility group box 1 (HMGB1) in RAW264.7 cells activated with lipopolysaccharide (LPS) in vitro and in LPS-or cecal ligation and puncture (CLP)-induced septic mice in vivo, so that HO-1 induction or CO improves survival of sepsis in rodents. We found that pretreatment with HO-1 inducers (hemin, cobalt protoporphyrin IX) or transfection of HO-1 significantly inhibited HMGB1 release, which was blocked by HO-1 small interfering RNA, in cells activated by LPS. Carbon monoxide-releasing molecule 2 (CORM-2) but not bilirubin or deferoxamine inhibited HMGB1 release in LPS-activated macrophages. Oxyhemoglobin reversed the effect of HO-1 inducers on HMGB1 release. Translocation of HMGB1 from nucleus to cytosol was significantly inhibited by HO-1 inducers, CORM-2, or HO-1 transfection. Neutralizing antibodies to tumor necrosis factor (TNF)-␣, interleukin (IL)-1␤, interferon-␤, and N -nitro-L-arginine methyl ester hydrochloride but not N-[2-(cyclohexyloxyl)-4-nitrophenyl]-methane sulfonamide (NS-398) significantly inhibited HMGB1 release in LPS-activated cells. Production of TNF-␣, IL-1␤, and IFN-␤ was significantly reduced by pretreatment of HO-1 inducers, CORM-2, or HO-1 transfection in LPS-activated cells. Plasma levels of HMGB1 in mice challenged with LPS or CLP were significantly reduced by the administration of HO-1 inducers or CORM-2, which was accompanied by either reduction (pretreatment) or no change (delayed administration) of serum TNF-␣ and IL-1␤ levels. Regardless of pretreatment or delayed administration, CORM-2 and hemin rescued mice from lethal endotoxemia and sepsis induced by LPS or CLP. Taken together, we concluded that HO-1-derived CO reduces HMGB1 release in LPS-activated cells and LPS-or CLP-induced animal model of sepsis.Sepsis is defined as a systemic inflammatory response syndrome from a microbial infection that results from excessive stimulation of the host immune system by pathogen components to produce various proinflammatory cytokines, and their overproduction causes systemic inflammation that can lead to the lethal multiple organ damage (Oberholzer et al., 2001). High-mobility group box 1 (HMGB1) is a chromatin-binding protein that participates in maintaining nucleosome structure and regulation of gene transcription (Landsman and Bustin, 1993). Various evidence indicated that HMGB1 is a necessary and sufficient late mediator of severe sepsis (Wang et al., 1999;Yang et al., 2004). Once released, HMGB1 can bind to cell-surface receptors, such as the receptor for advanced glycation end products and Toll-like receptors 2 and 4, and mediate various cellular responses, chemotactic cell movement, and release of proinflammatory Article, publication date, and citation information can be found at http://molpharm.aspetjournals.org. doi:10.1124/mol.109.055137.ABBREVIATIONS: HMGB1, high-mobility group box 1; HO-1, heme-oxygenase-1; CORM-2, carbon monoxide-releasing molecule II; LPS, lip...

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Section: Co Inhibits Hmgb1 Release In Lps-and Clp-induced Sepsis 179supporting

confidence: 90%

Section: Co Inhibits Hmgb1 Release In Lps-and Clp-induced Sepsis 179supporting

confidence: 90%

Section: Interleukin (Il)-1␤ Interferon-␤ and N -Nitro-l-arginine Msupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Heme-Oxygenase-1 Induction and Carbon Monoxide-Releasing Molecule Inhibit Lipopolysaccharide (LPS)-Induced High-Mobility Group Box 1 Release in Vitro and Improve Survival of Mice in LPS- and Cecal Ligation and Puncture-Induced Sepsis Model in Vivo

Tsoyi

Lee²,

Lee³

et al. 2009

Mol Pharmacol

180

110

View full text Add to dashboard Cite

show abstract

“…73 A recent study demonstrated that high-mobility group box 1 contributes to lethality of endotoxemia in HO-1-deficient mice. 74 A significant reduction of high-mobility group box 1 was noted after administration of carbon monoxide and biliverdin, products of the HO-1 enzymatic pathway. Moreover, HO-1 suppresses the infiltration of neutrophils in rat liver during sepsis.…”

Section: Therapeutic Options For the Present And Futurementioning

confidence: 97%

Sepsis and Acute Kidney Injury

Zarjou

Agarwal

2011

Journal of the American Society of Nephrology

461

363

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Acute Lung Injury and Pulmonary Vascular Permeability: Use of Transgenic Models

Parker

2011

Comprehensive Physiology

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Acute lung injury is a general term that describes injurious conditions that can range from mild interstitial edema to massive inflammatory tissue destruction. This review will cover theoretical considerations and quantitative and semi-quantitative methods for assessing edema formation and increased vascular permeability during lung injury. Pulmonary edema can be quantitated directly using gravimetric methods, or indirectly by descriptive microscopy, quantitative morphometric microscopy, altered lung mechanics, high-resolution computed tomography, magnetic resonance imaging, positron emission tomography, or x-ray films. Lung vascular permeability to fluid can be evaluated by measuring the filtration coefficient (Kf) and permeability to solutes evaluated from their blood to lung clearances. Albumin clearances can then be used to calculate specific permeability-surface area products (PS) and reflection coefficients (σ). These methods as applied to a wide variety of transgenic mice subjected to acute lung injury by hyperoxic exposure, sepsis, ischemia-reperfusion, acid aspiration, oleic acid infusion, repeated lung lavage, and bleomycin are reviewed. These commonly used animal models simulate features of the acute respiratory distress syndrome, and the preparation of genetically modified mice and their use for defining specific pathways in these disease models are outlined. Although the initiating events differ widely, many of the subsequent inflammatory processes causing lung injury and increased vascular permeability are surprisingly similar for many etiologies.

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High-Mobility Group Box 1 Contributes to Lethality of Endotoxemia in Heme Oxygenase-1–Deficient Mice

Cited by 65 publications

References 48 publications

Heme-Oxygenase-1 Induction and Carbon Monoxide-Releasing Molecule Inhibit Lipopolysaccharide (LPS)-Induced High-Mobility Group Box 1 Release in Vitro and Improve Survival of Mice in LPS- and Cecal Ligation and Puncture-Induced Sepsis Model in Vivo

Heme-Oxygenase-1 Induction and Carbon Monoxide-Releasing Molecule Inhibit Lipopolysaccharide (LPS)-Induced High-Mobility Group Box 1 Release in Vitro and Improve Survival of Mice in LPS- and Cecal Ligation and Puncture-Induced Sepsis Model in Vivo

Sepsis and Acute Kidney Injury

Acute Lung Injury and Pulmonary Vascular Permeability: Use of Transgenic Models

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