Cutting Edge: High-Mobility Group Box 1 Preconditioning Protects against Liver Ischemia-Reperfusion Injury

Izuishi, Kunihiko; Tsung, Allan; Jeyabalan, Geetha; Critchlow, Nathan D.; Li, Jianhua; Tracey, Kevin J.; DeMarco, Richard; Lotze, Michael T.; Fink, Mitchell P.; Geller, David A.; Billiar, Timothy R.

doi:10.4049/jimmunol.176.12.7154

Cited by 111 publications

(117 citation statements)

References 28 publications

(30 reference statements)

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“…27 In contrast to the proinflammatory role of HMGB1, preconditioning with HMGB1 provides protection against liver ischemia-reperfusion injury. 36 HMGB1 is a distal mediator of acute inflammatory lung injury. HMBG1 given intratracheally caused acute inflammatory injury to the lungs with neutrophil accumulation, the development of lung edema, and increased pulmonary production of IL-1␤, TNF␣, and MIP-2, whereas administration of anti-HMGB1 Abs reduced the lung injury in endotoxin-induced acute lung inflammation.…”

Section: Discussionmentioning

confidence: 99%

HMGB1 Contributes to Kidney Ischemia Reperfusion Injury

Wang

et al. 2010

Journal of the American Society of Nephrology

305

259

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High-mobility group box 1 (HMGB1), a nuclear factor released extracellularly as an inflammatory cytokine, is an endogenous ligand for Toll-like receptor 4 (TLR4). TLR4 activation mediates kidney ischemia-reperfusion injury (IRI), but whether HMGB1 contributes to IRI is unknown. Here, treating wild-type mice with neutralizing anti-HMGB1 antibody protected them against kidney IRI, evidenced by lower serum creatinine and less tubular damage than untreated mice. Mice treated with anti-HMGB1 had significantly less tubulointerstitial infiltration by neutrophils (day 1) and macrophages (day 5) and markedly reduced apoptosis of tubular epithelial cells. Furthermore, anti-HMGB1 antibody-treated IRI kidneys had significantly lower levels of IL-6, TNF␣, and monocyte chemoattractant protein 1 (MCP1). mRNA, which are downstream of HMGB1. Conversely, administration of rHMGB1 after reperfusion exacerbated kidney IRI in wild-type mice. TLR4 deficient (TLR4 Ϫ/Ϫ ) mice were protected against kidney IRI; administration of neither anti-HMGB1 antibody nor rHMGB1 affected this renoprotection. In conclusion, endogenous HMGB1 promotes kidney damage after IRI, possibly through the TLR4 pathway. Administration of a neutralizing antibody to HMGB1 either before or soon after ischemia-reperfusion affords significant protection, suggesting therapeutic potential for acute kidney injury.

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Section: Discussionmentioning

confidence: 99%

HMGB1 Contributes to Kidney Ischemia Reperfusion Injury

Wang

et al. 2010

Journal of the American Society of Nephrology

305

259

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“…Recent studies show that Bβ15-42 (the fibrin-derived peptide), PNU-282987 (a selective α7 nicotinic acetylcholine receptor agonist), EPC-K1 (the vitamin E derivative), melatonin, cisplatin and glycyrrhizin attenuate warm liver I/R damage partly through inhibition of HMGB1 release (47)(48)(49)(50)(51)(52). Interestingly, pretreatment of mice with HMGB1 protein significantly decreased liver I/R injury through upregulation of IL-1R-associated kinase-M, a negative regulator of TLR4 signaling (53). Thus, extracellular HMGB1 may have a dual role in regulation of hepatic I/R injury, which depends on its posttranslational modifications and receptors.…”

Section: Hmgb1 and Liver I/rmentioning

confidence: 99%

Emerging Role of High-Mobility Group Box 1 (HMGB1) in Liver Diseases

Chen

Hou

Zhang

et al. 2013

Mol Med

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Damage-associated molecular pattern (DAMP) molecules are essential for the initiation of innate inflammatory responses to infection and injury. The prototypic DAMP molecule, high-mobility group box 1 (HMGB1), is an abundant architectural chromosomal protein that has location-specific biological functions: within the nucleus as a DNA chaperone, within the cytosol to sustain autophagy and outside the cell as a DAMP molecule. Recent research indicates that aberrant activation of HMGB1 signaling can promote the onset of inflammatory and autoimmune diseases, raising interest in the development of therapeutic strategies to control their function. The importance of HMGB1 activation in various forms of liver disease in relation to liver damage, steatosis, inflammation, fibrosis, tumorigenesis and regeneration is discussed in this review.

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“…The affinity purification of the polyclonal anti-HMGB1 Ab was performed as previously reported (15). To affinity purify HMGB1, 10 ml of freshly prepared and filtered HeLa lysate was loaded onto the rabbit polyclonal anti-HMGB1 affinity column and recirculated for 30 min.…”

Section: Hmgb1 Polyclonal Abmentioning

confidence: 99%

Eosinophils Oxidize Damage-Associated Molecular Pattern Molecules Derived from Stressed Cells

Lotfi

Herzog

DeMarco

et al. 2009

The Journal of Immunology

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Eosinophils (Eos) are found at increased numbers within necrotic areas of tumors. We show that necrotic material from cell lysates containing damage-associated molecular pattern molecules induce eosinophil degranulation (release of major basic protein and eosinophil peroxidase) and enhance their oxidative burst while the stimulatory capacity of cell lysates is significantly diminished following oxidation. High mobility group box 1 (HMGB1), a prototypic damage-associated molecular pattern molecule, released following necrosis but not apoptosis, induced a similar effect on Eos. Additionally, we demonstrate that HMGB1 enhances eosinophil survival and acts as a chemoattractant. Consistently, we show that Eos express an HMGB1 receptor, the receptor for advanced glycation end product, and that anti-receptor for advanced glycation end product could diminish the HMGB1-mediated effects. Of all tested biologic activities, Eos respond most sensitively to the presence of necrotic material including HMGB1 with generation of peroxide. We postulate that Eos “sense” necrotic cell death, migrating to and responding to areas of tissue injury/necrosis. Oxidation of cell lysates reduces their biologic activity when compared with native lysates. We postulate that eosinophil-associated modulation of immunity within tumor and other damaged tissues may be primarily by promoting oxidative degradation of necrotic material. Novel therapeutic strategies may be considered by advancing oxidative denaturation of released necrotic material using Eos or other aerobic strategies.

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Cutting Edge: High-Mobility Group Box 1 Preconditioning Protects against Liver Ischemia-Reperfusion Injury

Cited by 111 publications

References 28 publications

HMGB1 Contributes to Kidney Ischemia Reperfusion Injury

HMGB1 Contributes to Kidney Ischemia Reperfusion Injury

Emerging Role of High-Mobility Group Box 1 (HMGB1) in Liver Diseases

Eosinophils Oxidize Damage-Associated Molecular Pattern Molecules Derived from Stressed Cells

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