High mobility box 1 mediates neutrophil recruitment in myocardial ischemia–reperfusion injury through toll like receptor 4-related pathway

Ding, Hua‐Sheng; Yang, Jun; Gong, Feili; Yang, Jian; Ding, Jiawang; Song, Li; Jiang, Yurong

doi:10.1016/j.gene.2012.07.072

Cited by 38 publications

(22 citation statements)

References 26 publications

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“…CXCR4 is implicated in lymphocyte (17) and neutrophil chemotaxis (18) from the periphery. CXCR4 can engage CXCL12 as a homodimer or a 2:1 heterocomplex of CXCL12 and HMGB1, the latter serving as a danger signal during immunogenic cell death (19,20). …”

Section: Resultsmentioning

confidence: 99%

Cabozantinib Eradicates Advanced Murine Prostate Cancer by Activating Antitumor Innate Immunity

et al. 2017

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Several kinase inhibitors that target aberrant signaling pathways in tumor cells have been deployed in cancer therapy. However, their impact on the tumor immune microenvironment remains poorly understood. The tyrosine kinase inhibitor cabozantinib showed striking responses in cancer clinical trial patients across several malignancies. Here we show that cabozantinib rapidly eradicates invasive, poorly-differentiated PTEN/p53 deficient murine prostate cancer. This was associated with enhanced release of neutrophil chemotactic factors from tumor cells, including CXCL12 and HMGB1, resulting in robust infiltration of neutrophils into the tumor. Critically, cabozantinib-induced tumor clearance in mice was abolished by antibody-mediated granulocyte depletion or HMGB1 neutralization or blockade of neutrophil chemotaxis with the CXCR4 inhibitor, plerixafor. Collectively, these data demonstrate that cabozantinib triggers a neutrophil-mediated anti-cancer innate immune response, resulting in tumor clearance.

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Section: Resultsmentioning

confidence: 99%

Cabozantinib Eradicates Advanced Murine Prostate Cancer by Activating Antitumor Innate Immunity

et al. 2017

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“…Besides exerting its function in the nucleus, extracellular HMGB1 can mediate various physical or pathological processes, including stimulating inflammatory factor expression and release mainly by binding to its specific receptors, such as RAGE, TLR-2 and TLR-4 (32). Therefore, HMGB1 has been recognized as an important pro-inflammatory mediator and is important in initiating and amplifying the inflammatory response (9–12). In addition, it has been reported that the HMGB1-triggered inflammatory response is crucial in myocardial I/R injury since a decrease in HMGB1 expression and release could significantly inhibit the inflammatory response and ameliorate I/R-induced myocardial injury (11,33).…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies demonstrated that extracellular HMGB1 is a potent pro-inflammatory mediator (9,10), and is important in triggering the inflammatory response during myocardial I/R (11,12). Furthermore, it has been reported that HMGB1 exerts its pro-inflammatory effects via its specific receptors, which mainly include a receptor for advanced glycation end products (RAGE), Toll-like receptor (TLR)-2 and TLR-4 (13).…”

Section: Introductionmentioning

confidence: 99%

Picroside II protects myocardium from ischemia/reperfusion-induced injury through inhibition of the inflammatory response

Meiqing

et al. 2016

Experimental and Therapeutic Medicine

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The inflammatory response is important in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Picroside II, the primary active constituent of Picrorhizae, has been reported to protect the myocardium from I/R-induced injury, however, the exact mechanism underlying these protective effects remains unclear. The aim of the present study was to investigate the mechanism underlying the protective effects of picroside II on I/R-induced myocardial injury. Adult male Sprague-Dawley rats underwent 1 h left coronary artery occlusion followed by 3 h reperfusion. Picroside II was administered (10 mg/kg) via the tail vein 30 min prior to left coronary artery occlusion. The results revealed that pretreatment of picroside II could significantly alleviate I/R-induced myocardial injury concomitantly with a decrease in inflammatory factor production. In addition, picroside II was also able to decrease high mobility group box 1 (HMGB1) expression, and release and downregulate the expression of the receptor for advanced glycation end products (RAGE), toll-like receptor (TLR)-2 and TLR-4. Furthermore, picroside II was able to inhibit nuclear factor-κB (NF-κB) activation. The results indicated that the protective effect of picroside II on I/R-induced myocardial injury was associated, at least partly, with inhibition of the inflammatory response by suppressing the HMGB1-RAGE/TLR-2/TLR-4-NF-κB signaling pathway.

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“…Similarly, the possible involvement of HMGB1 in the increased expression of vascular endothelial adhesion molecules, which play a critical role in cell recruitment, was demonstrated. Because HMGB1 is shown to have direct chemoattractant ability in recruiting neutrophils and mononuclear leukocytes [18,30], it may be a key player in the vicious cycle of inflammation through inflammatory cell migration.…”

Section: Discussionmentioning

confidence: 99%

Recombinant Thrombomodulin Modulates Murine Colitis Possibly via High-Mobility Group Box 1 Protein Inhibition

Ueda¹,

Higashiyama²,

Narimatsu³

et al. 2015

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Background and Aim: Thrombomodulin (TM) is an anticoagulant cofactor protein. We hypothesized that its recombinant soluble TM (rhTM) form, widely used to treat disseminated intravascular coagulation, might have anti-inflammatory action in inflammatory bowel disease (IBD), possibly through its inhibition of high-mobility group box 1 protein (HMGB1). Methods: We investigated inflammatory effects of HMGB1 and anti-inflammatory effect of rhTM in dextran sulfate sodium (DSS)-treated mice, some cell lines and ulcerative colitis (UC) patients, particularly focusing on changes of vascular endothelial adhesion molecules. Results: Treatments with rhTM significantly attenuated DSS-treated mice clinically and histologically. The mRNA levels of proinflammatory cytokines and adhesion molecules were decreased by rhTM. Increased inflammatory cells in the colonic mucosa strongly expressed HMGB1 in the cytoplasm in the DSS-treated mice and UC patients' colonic mucosa, which were significantly decreased by rhTM in mice. In in vitro experiments, rhTM significantly decreased the mRNA levels of tumor necrosis factor-alpha (TNF-α) and adhesion molecules increased by endotoxin exposures in RAW 264.7 (macrophage cell line) and bEND.3 cells (endothelial cell line), suggesting the proinflammatory role of HMGB1 in TNF-α production from macrophages. Conclusions: These findings suggest that rhTM may be useful for the treatment of IBD by attenuating inflammatory cytokine production and adhesion molecule expression, partly because of its inhibition of HMGB1.

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High mobility box 1 mediates neutrophil recruitment in myocardial ischemia–reperfusion injury through toll like receptor 4-related pathway

Cited by 38 publications

References 26 publications

Cabozantinib Eradicates Advanced Murine Prostate Cancer by Activating Antitumor Innate Immunity

Cabozantinib Eradicates Advanced Murine Prostate Cancer by Activating Antitumor Innate Immunity

Picroside II protects myocardium from ischemia/reperfusion-induced injury through inhibition of the inflammatory response

Recombinant Thrombomodulin Modulates Murine Colitis Possibly via High-Mobility Group Box 1 Protein Inhibition

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