Granulomatous nephritis can be triggered by diverse factors and results in kidney failure. However, despite accumulating data about granulomatous inflammation, pathogenetic mechanisms in nephritis remain unclear. The DNA-binding high-mobility group box-1 protein (HMGB1) initiates and propagates inflammation when released by activated macrophages, and functions as an alarm cytokine signaling tissue damage. In this study, we showed elevated HMGB1 expression in renal granulomas in rats with crystal-induced granulomatous nephritis caused by feeding an adenine-rich diet. HMGB1 levels were also raised in urine and serum, as well as in monocyte chemoattractant protein-1 (MCP-1), a mediator of granulomatous inflammation. Injection of HMGB1 worsened renal function and upregulated MCP-1 in rats with crystal-induced granulomatous nephritis. HMGB1 also induced MCP-1 secretion through mitogen-activated protein kinase (MAPK) and phosphoinositide-3-kinase (PI3K) pathways in rat renal tubular epithelial cells ...
Background: High-mobility group box 1 (HMGB1) is an endogenous molecule released during cell stress and death termed damage-associated molecular patterns (DAMPs). HMGB1 activates the pattern recognition receptor, toll-like receptor 4 (TLR4), and induces sterile inflammation. However, how HMGB1 and TLR4 affect restenosis, the major complication following balloon and stent intervention clinically, remains unknown. We tested the hypothesis that HMGB1 released following acute arterial injury promotes intimal hyperplasia (IH), a hallmark of restenosis, via TLR4 signaling pathway.. Methods and Results: Wire injury of the carotid artery in C57BL/6 wild-type (WT) mice significantly increased intima-to-media ratio in 4 weeks. Global deletion of HMGB1 using an inducible knockout mouse strain prevented IH and vessel remodeling. IH decreased by over 50% in WT mice treated with a HMGB1 neutralizing antibody. Of the mouse strains deficient in putative receptors and co-regulator for HMGB1 (TLR4-/-, TLR2-/-, ...
TY - JOUR. T1 - Contributions of high mobility group box protein in experimental and clinical acute lung injury. AU - Ueno, Hiroshi. AU - Matsuda, Tomoyuki. AU - Hashimoto, Satoru. AU - Amaya, Fumimasa. AU - Kitamura, Yoshihiro. AU - Tanaka, Masaki. AU - Kobayash, Atsuko. AU - Maruyama, Ikuro. AU - Yamada, Shingo. AU - Hasegawa, Naoki. AU - Soejima, Junko. AU - Koh, Hidefumi. AU - Ishizaka, Akitoshi. PY - 2004/12/15. Y1 - 2004/12/15. N2 - This study was performed to examine the putative role of high mobility group box (HMGB) protein in the pathogenesis of acute lung injury (ALI). Observations were made (7) in 21 patients who were septic with ALI and 15 patients with normal lung function and (2) in a mouse model 24 hours after intratracheal instillation of lipopolysaccharide (LPS). The concentrations of HMGB1 were increased in plasma and lung epithelial lining fluid of patients with ALI and mice instilled with LPS. LPS-induced ALI was mitigated by anti-HMGB1 antibody. Although this protein was ...
HMGB1 (high-mobility group box 1) protein, a pleiotropic cytokine released by several cell types under physiological and pathological conditions, has been identified as a signal molecule active on A431 cells. Although extracellular HMGB1 itself does not trigger any detectable signalling effect on these cells, it induces an increased susceptibility to EGF (epidermal growth factor) stimulation. Specifically, at concentrations of EGF which promote undetectable or limited cell responses, the addition of sub-nanomolar concentrations of HMGB1 potentiates the effect of EGF by specifically activating a downstream pathway that leads to enhanced cell motility through an increase in Ca2+ influx, activation of extracellular-signal-regulated kinase 1/2 and remodelling of the actin cytoskeleton. These results, which identify extracellular HMGB1 as an activator of human tumour cell migration operating in concert with EGF, have important implications in the search for novel strategies to control tumour ...
TY - JOUR. T1 - Interaction Analysis Between Polyglutamine-expanded TATA Box Binding Protein (TBP) and High Mobility Group Box 1 (HMGB1). AU - 楊, 淑婷(Shu-Ting Yang). AU - 陳, 襄銘(Hsiang-Ming Chen). AU - 李, 麗卿(Li-Ching Lee). AU - 黃, 詩涵(Shih-Han Huang). AU - 林, 志信(Chih-Hsin Lin). AU - 李, 冠群(Guan-Chiun Lee). AU - 李, 振綱(Cheng-Kang Lee). AU - 李, 桂楨(Guey-Jen Lee-Chen). PY - 2013. Y1 - 2013. N2 - 第十七型脊髓小腦共濟失調症(SCA17)與轉錄起始因子TATA binding protein (TBP)基因上的多麩醯胺擴增相關。TBP與包括high mobility group box 1 (HMGB1)在內的其他蛋白因子交互作用,來調節基因的表現。本研究藉重組的HMGB1 及TBP/Q20~61 N端蛋白,探討TBP Q長度是否影響其與HMGB1的結合。首先共表現HMGB1及TBP於 HEK-293細胞後,利用免疫共沉澱及GST pull-down試驗,確認HMGB1 與TBP在細胞內的結合。其次原核E. coli表現的重組HMGB1 ...
Human malignant gliomas, the most common primary brain tumors, are characterized by excessive proliferation and infiltrative growth. Although the molecular determinants of glioma properties are still unclear, a significant role for the altered regulation of modulators of glial growth and motility has been proposed. In the complex network of molecular signals involved in tumorigenesis, high mobility group box 1 protein (HMGB1) has recently emerged. This low molecular weight protein, previously considered solely as a chromatin-associated molecule, can be present extracellularly after passive release by necrotic cells or active secretion by some cell types. In the extracellular milieu, HMGB1 can act as a multifunctional paracrine/autocrine factor via its interaction with the receptor for advanced glycation end products (RAGE). Increasing evidence supports that HMGB1 plays an important role in tumors, promoting cancer cell growth, motility, and invasion. Although different human tumors overexpress ...
IV Vitamin C Stops Sepsis in Its Tracks. Reference: NPR, Chest, Managed Care, Barry Fowler, Biofactors,. The number three cause of death in America today is the overwhelming infection that causes blood pressure collapse, kidney shut down and death called sepsis. Three hundred thousand people in America die from it each year. As far is deaths in hospitals, its number one. Sepsis is dangerous.. The cause of sepsis is still not exactly known, but it acts like a runaway train. "Cytokine storm" is the term used to describe the same process in severe influenza, where all your hormones of inflammation fire off in a cycle of uncontrolled and dysfunctional activation. One thing in known, there is a leaking of capillaries all over the body while alarmins (danger-associated molecular patterns (DAMPs)) are released. These DAMPs are nuclear, cytoplasmic, or mitochondria structures that acquire new functions outside the cell. Examples of DAMPs have great names like high mobility group box-1 protein HMGB1, ...
Acetaminophen (APAP) overdose induces massive hepatocyte necrosis. Necrotic tissue releases high mobility group B1 (HMGB1), and HMGB1 contributes to liver injury. Even though blockade of HMGB1 does not protect against APAP-induced acute liver injury (ALI) at 9 h time point, the later time points are not studied and the role of HMGB1 in APAP overdose is unknown, it is possible that neutralization of HMGB1 might improve hepatocyte regeneration. This study aims to test whether blockade of HMGB1 improves hepatocyte regeneration after APAP overdose. Male C57BL/6 mice were treated with a single dose of APAP (350 mg/kg). 2 hrs after APAP administration, the APAP challenged mice were randomized to receive treatment with either anti-HMGB1 antibody (400 μg per dose) or non-immune (sham) IgG every 24 hours for a total of 2 doses. 24 hrs after APAP injection, anti-HMGB1 therapy instead of sham IgG therapy significantly improved hepatocyte regeneration microscopically; 48 hrs after APAP challenge, the sham IgG
Background: High Mobility Group Box 1 (HMGB1) is as an abundant and ubiquitous nuclear DNA-binding protein that has multiple functions dependent on its cellular location. In the nucleus, HMGB1 binds to DNA and is critical for proper transcriptional regulation. However, little is known about the effects of HMGB1 on heart failure. The aim of this study was to examine the impact of HMGB1 on cardiac dysfunction induced by pressure overload.. Methods and Results: We generated transgenic mice with cardiac-specific overexpression of HMGB1 (HMGB1-TG) using α-myosin heavy chain promoter. There were no differences in cardiac morphology and function between wild-type (WT) and HMGB1-TG mice at basal condition. Thoracic transverse aortic constriction (TAC) was performed in transgenic mice with cardiac-specific overexpression of HMGB1 (HMGB1-TG) and wild-type (WT) mice. The survival rate after TAC was significantly higher in HMGB1-TG mice compared to WT mice. Increases in heart/body weight ratio after TAC ...
Background: Smokers show increased prevalence of insulin resistance for glucose and type 2 diabetes mellitus (T2DM). The underlying mechanisms, however, remain poorly understood. Tobacco smoke exposure increases tissue expression of high mobility group box 1 (HMGB1), a damage-associated molecular pattern (DAMP) that activates innate immunity. We recently reported that exposure of human macrophages to tobacco smoke extract (TSE) provokes the release of HMGB1 in two forms: as a soluble molecule and carried on membrane microvesicles (MV). Both soluble recombinant HMGB1 (rHMGB1) and MV-associated HMGB1 on TSE-induced MVs (TSE-MVs) mediate crucial crosstalk with adipocytes by impairing insulin signaling and by recruiting monocytes to the adipocytes -. GOAL- To identify the receptors on adipocytes that mediate the effects of HMGB1 on insulin signaling and monocyte recruitment.. Methods: Cultured 3T3-L1 adipocytes were incubated for 24h with rHMGB1 or TSE-MVs, in the absence or presence of neutralizing ...
Postoperative neurocognitive disorders are common complications in elderly patients following surgery or critical illness. High mobility group box 1 protein (HMGB1) is rapidly released after tissue trauma and critically involved in response to sterile injury. Herein we assessed the role of HMGB1 after liver surgery in aged rats and explored the therapeutic potential of a neutralizing anti-HMGB1 monoclonal antibody in a clinically relevant model of postoperative neurocognitive disorders. 19-22 months Sprague Dawley rats were randomly assigned as: (1) control with saline; (2) surgery, a partial hepatolobectomy under sevoflurane anesthesia and analgesia, + immunoglobulin G as control antibody; (3) surgery + anti-HMGB1. A separate cohort of animals was used to detect His-tagged HMGB1 in the brain. Systemic anti-HMGB1 antibody treatment exerted neuroprotective effects preventing postoperative memory deficits and anxiety in aged rats by preventing surgery-induced reduction of phosphorylated cyclic AMP
TY - JOUR. T1 - Exogenous high-mobility group box 1 improves myocardial recovery after acute global ischemia/reperfusion injury. AU - Abarbanell, Aaron M.. AU - Hartley, Jacob A.. AU - Herrmann, Jeremy L.. AU - Weil, Brent R.. AU - Wang, Yue. AU - Manukyan, Mariuxi C.. AU - Poynter, Jeffrey A.. AU - Meldrum, Daniel R.. PY - 2011/3/1. Y1 - 2011/3/1. N2 - Background: High-mobility group box 1 (HMGB1) is a mediator of inflammation with dose-dependent effects. In the setting of regional myocardial infarction, a high-dose HMGB1 treatment decreases myocardial function, whereas low-dose HMGB1 improves function; however, it is unknown what role HMGB1 has in the setting of global ischemia/reperfusion (I/R) injury. We hypothesized that a low-dose HMGB1 treatment would improve myocardial functional recovery and decrease infarct size after global I/R injury in association with increased levels of cardioprotective paracrine factors and decreased inflammation. Methods: Adult rat hearts were isolated and ...
Summary: Tissue damage occurs often in the life of mammals and is usually repaired. Dying cells are swiftly phagocytosed, but before disappearing, they alert surrounding cells to activate homeostatic programs. They release signals that recruit inflammatory cells to the site of injury, promote cell migration and cell division to replace dead cells, and activate the immune system in anticipation of microbial invasion. Many of these events involve high-mobility group box 1 protein (HMGB1), a nuclear protein that is released passively when necrotic cells lose the integrity of their membranes. HMGB1 behaves as a trigger of inflammation, attracting inflammatory cells, and of tissue repair, recruiting stem cells and promoting their proliferation. Moreover, HMGB1 activates dendritic cells (DCs) and promotes their functional maturation and their response to lymph node chemokines. Activated leukocytes actively secrete HMGB1 in the microenvironment. Thus, HMGB1 acts in an autocrine/paracrine fashion and ...
REPORT High Mobility Group Protein B1 (High Mobility Group Protein 1 or High Mobility Group Protein Box 1 or HMGB1) - High mobility group box 1 protein also known as high-mobility group protein 1 (HMG-1) is a protein encoded by ... > ...
The majority of glutathione, an important antioxidant, appears in the body in its reduced form (GSH), with 10% appearing in its oxidized form of glutathione disulfide (GSSG). A deficiency in glutathione results in oxidative stress and plays a major role in the pathogenesis of type 2 diabetes. Furthermore, oxidative stress is an important cause of intestinal epithelial cell death. High mobility group box 1 protein (HMGB1) has been shown to mitigate disease and inhibit apoptosis. This investigation sought to determine the effect of HMGB1 on oxidative stress in the gut to determine HMGB1s role in the pathogenesis of type 2 diabetes. The oxidative stress of HMGB1 f/f and HMGB1 f/f vil-CRE mice was measured using a GSH/GSSG ratio assay kit on ileal mucosal scrapings, cecal contents, stoop samples, and tissue taken from the liver. Future investigations could investigate the role of HMGB1 in conjunction with diet by also using mice that are fed either a high fat diet or a regular chow diet.
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Abcam provides specific protocols for Anti-HMGB1 antibody - ChIP Grade (ab18256) : ChIP protocols, Immunoprecipitation protocols, Immunohistochemistry…
Systemic lupus erythematosus (SLE) is a systemic inflammatory disease. Clinically, the distinction between ongoing inflammation attributed to SLE, and organ damage due to medication or co-morbidities remains challenging. In addition, SLE is a heterogeneous disease where the various disease phenotypes complicate the search for biomarkers that adequately reflect disease activity and/or signs of increasing organ damage. The aim of the thesis was to investigate and evaluate potential new biomarkers of disease activity and/or organ damage in SLE patients.. High mobility group box protein-1 (HMGB1) is a nuclear non-histone protein that can shuttle to the cytoplasm, become secreted extracellularly, and participate in systemic inflammation. Administration of monoclonal anti-HMGB1 antibodies has been reported both to attenuate and intensify disease in animal models of arthritis and lupus. In Paper I of the thesis, circulating anti-HMGB1 was found in 23% of the SLE patients and correlated with disease ...
Innate immune mechanisms represent bodys first line of defense against pathogens, capable of recognizing Pathogen-associated molecular patterns (PAMPs) and Damage-associated molecular pattern molecules (DAMPs). The PAMPs and DAMPs are recognized by pattern recognition receptors (PRRs), such as membrane bound Toll-like receptors (TLRs) or cytoplasmic NOD-like receptors (NLR) and RIG-I- like receptors (RLR). This page provides a broad review of the signaling pathways for these receptors leading to inflammation and immune activation. BioLegend develops and manufactures world-class, cutting-edge immunological reagents for biomedical research, offered at an outstanding value.
Patients surviving sepsis develop anemia but the molecular mechanism is unknown. Here we observed that mice surviving polymicrobial Gram-negative sepsis develop hypochromic, microcytic anemia with reticulocytosis. The bone marrow of sepsis survivors accumulates polychromatophilic and orthochromatic erythroblasts. Compensatory extramedullary erythropoiesis in the spleen is defective during terminal differentiation. Circulating TNF and IL-6 are elevated for five days after the onset of sepsis, and serum HMGB1 levels are increased from day seven until at least day 28. Administration of recombinant HMGB1 to healthy mice mediates anemia with extramedullary erythropoiesis and significantly elevated reticulocyte counts. Moreover, administration of anti-HMGB1 monoclonal antibodies after sepsis significantly ameliorates the development of anemia (hematocrit 48.5+/-9.0% versus 37.4+/-6.1%, p
In study III, the association between plasma HMGB1 and objective cognitive function measured in four different cognitive domains (executive function, visual memory, sustained attention, working memory) was investigated. Interestingly, plasma levels of HMGB1 were significantly elevated in the ICU, at discharge, and at the three- and six-months follow-up visits as compared with reference popula- tions. Elevated plasma levels of HMGB1 were associated with reduced sustained attention at the three- and six-month follow-up visits. Based on these findings, further follow-up studies on HMGB1 biology in ICU survivors are warranted to investigate the potential for therapeutic targeting of HMGB1 function in preven- tion of cognitive impairment in ICU survivorsIn study IV we explore the association between plasma HMGB1 and physical performance at ICU follow-up. We observed no significant association between levels of plasma HMGB1 and the three physical tests performed (i.e., 6-min walk test, timed stands ...
High-mobility group box 1 (HMGB1) is an important molecule for several nuclear processes. Recently, HMGB1 has gained much attention as a damage-associated molecular pattern (DAMP) and has been...
High mobility group box B (HMGB) proteins are pivotal in the development of cancer. Although the proteomics of prostate cancer (PCa) cells has been reported, the involvement of HMGB proteins and their interactome in PCa is an unexplored field of considerable interest. We describe herein the results of the first HMGB1/HMGB2 interactome approach to PCa. Libraries constructed from the PCa cell line, PC-3, and from patients’ PCa primary tumor have been screened by the yeast 2-hybrid approach (Y2H) using HMGB1 and HMGB2 baits. Functional significance of this PCa HMGB interactome has been validated through expression and prognosis data available on public databases. Copy number alterations (CNA) affecting these newly described HMGB interactome components are more frequent in the most aggressive forms of PCa: those of neuroendocrine origin or castration-resistant PCa. Concordantly, adenocarcinoma PCa samples showing CNA in these genes are also associated with the worse prognosis. These findings open the
Cette publication a donnée lieu à un commentaire dans la revue Immunity, 2008, 29(1): 1-2. Kazama H, Ricci JE, Herndon JM, Hoppe G, Green DR and Ferguson TA. Induction of immunological tolerance by apoptotic cells requires caspase-dependent oxidation of high-mobility group box-1 protein. Immunity, 2008, 29(1): 21-32.. Mastino A, Basu S, Brunner T, Ricci JE and Diederich M. Long live the cell death! Cell Death Differ, 2008, 15(8): 1330-1332. 2007 Colell, A.,* Ricci, J. E.,* Tait, S., Milasta, S., Maurer, U., Bouchier-Hayes, L., Fitzgerald, P., Guio-Carrion, A., Waterhouse, N. J., Wei Li, C., Mari, B., Barbry, P., Newmeyer, D. D.,. Beere, H. and Green, D. R. (2007) GAPDH and autophagy preserve cellular survival during caspase-independent cell death Cell, 129(5):983-997. *co-first author.. Cette publication a donnée lieu à des commentaires dans les revues Cell et Nature Cell Biology (Cell. 2007 Jun 1;129(5):861-3 -- Nat Cell Biol. (2007) Aug;9(8):869-70). Ricci, JE, Munoz-Pinedo, C, Fitzgerald, ...
Aim: To determine whether high-mobility group box 1 (HMGB1) and Toll like receptor 4 (TLR4) drive the inflammatory cascade that promotes intimal hyperplasia (IH) following acute vascular injury. Methods and Results: Carotid artery wire injury in C57BL/6 mice induced a significant increase in intima to media (I/M) ratio at four weeks. Global deletion of HMGB1 using an inducible knockout mouse strain caused prevention of IH. IH was decreased by over 50% in WT mice treated with HMGB1 neutralizing antibody. Of knockout mouse strains deficient in putative receptors for HMGB1, TLR4-/- mice showed the greatest inhibition of IH. Both anti-HMGB1 treated mice and TLR4-/- mice exhibited a marked decrease in monocytic recruitment. Mice with selective depletion of TLR4 from macrophage exhibited a similar level of inhibition of IH to that seen in the global TLR4-/-. In vitro, dithiol HMGB1 dose-dependently promoted SMC migration and MCP-1/CCR2 expression, which was abolished by TLR4 inhibitory peptide. ...
Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Cerebral edema, a life-threatening medical complication, contributes to elevated intracranial pressure (ICP) and a poor clinical prognosis after TBI. Unfortunately, treatment options to reduce post-traumatic edema re …
Discussion The importance of inflammatory response in the pathophysiology of ischemic stroke is generally recognized. HMGB1 has been identified as an early mediator of hemorrhage after acute lung injury [33] and hepatic injury after liver ischemia/reperfusion [34]. Recent evidence suggests that the inflammatory cytokine HMGB1 is an active mediator of ischemic brain injury [29]. Moreover, elevated levels of HMGB1 in the serum of human patients with cerebral infarction have also been reported [35]. Therefore, HMGB1 has been attracting attention as a potential diagnostic marker [36,37]. HMGB1 was identified as a ubiquitously expressed, abundant nonhistone DNA-binding protein, which stabilizes the nucleosome formation and facilitates gene transcription. HMGB1 protein can be actively released into the extracellular space by macrophages and monocytes [16,20]. It is also passively released by necrotic cells, although not by apoptotic cells, and it triggers inflammation [38]. Extracellular HMGB1 ...
PREDICTED: similar to High mobility group protein 1 (HMG-1) (High mobility group protein B1) (Amphoterin) (Heparin-binding protein p30) isoform 1 [Canis familiaris ...
Macrophage polarization is critical to inflammation and resolution of inflammation. We previously showed that high-mobility group box 1 (HMGB1) can engage receptor for advanced glycation end product (RAGE) to direct monocytes to a proinflammatory phenotype characterized by production of type 1 IFN and proinflammatory cytokines. In contrast, HMGB1 plus C1q form a tetramolecular complex cross-linking RAGE and LAIR-1 and directing monocytes to an antiinflammatory phenotype. Lipid mediators, as well as cytokines, help establish a milieu favoring either inflammation or resolution of inflammation. This study focuses on the induction of lipid mediators by HMGB1 and HMGB1 plus C1q and their regulation of IRF5, a transcription factor critical for the induction and maintenance of proinflammatory macrophages. Here, we show that HMGB1 induces leukotriene production through a RAGE-dependent pathway, while HMGB1 plus C1q induces specialized proresolving lipid mediators lipoxin A4, resolvin D1, and resolvin D2 through
Declining renal function is commonly observed with age. Obesity induced by a high-fat diet (HFD) may reduce renal function. Korean red ginseng (KRG) has been reported to ameliorate oxidative tissue injury and have an anti-aging effect. This study was designed to investigate whether HFD would accelerate the D-galactose-induced aging process in the rat kidney and to examine the preventive effect of KRG on HFD and D-galactose-induced aging-related renal injury. When rats with D-galactose-induced aging were fed an HFD for 9 wk, enhanced oxidative DNA damage, renal cell apoptosis, protein glycation, and extracellular high mobility group box 1 protein (HMGB1), a signal of tissue damage, were observed in renal glomerular cells and tubular epithelial cells ...
HMGB1 is a ubiquitous, abundant nuclear protein highly conserved among all mammals (11, 45). Incubation of macrophages with LPS or TNF-α results in increased release of HMGB1, and HMGB1 itself can stimulate macrophages, monocytes, and neutrophils to release proinflammatory cytokines, including IL-1β, TNF-α, and IL-8 (2, 30, 44). Increased circulating levels of HMGB1, attributed to release from activated macrophages, have been measured in the serum of mice treated with endotoxin as well as from septic patients (44). Additionally, HMGB1 appears to function as a late mediator of endotoxin lethality, as demonstrated by improved survival after treatment with specific anti-HMGB1 antibodies (44). When added to target cell cultures, HMGB1 can potently induce multiple responses, including differentiation, cytoskeletal reorganization, migration, and release of proinflammatory cytokines (1, 2, 9, 32). Recent information also suggests that HMGB1 may be an indicator of cell death by necrosis because its ...
Results presented herein provide new insights into the release of HMGB1 by macrophages in cells stimulated by TLR ligands and suggest that the translocation of this protein and apoptosis are closely related processes that may reflect common mechanisms. Thus, as our findings show, stimulation of RAW 264.7 cells by either LPS or poly(I:C) leads to the translocation of HMGB1 from the nucleus into the extracellular milieu under conditions in which the frequency of apoptotic cells increases dramatically; similar results were obtained with primary macrophages cultured from mice. Although the presence of apoptotic cells in cultures of activated cells does not prove that they are the source of HMGB1, the failure of cells stimulated by CpG DNA to release HMGB1 suggests that activation by itself is not sufficient for this process. Thus, for macrophages, it appears that apoptosis is closely associated with events leading to HMGB1 release and, indeed, may be the origin of at least some of the HMGB1 released ...
HMGB3 silence inhibits breast cancer cell proliferation and tumor growth by interacting with hypoxia-inducible factor 1alpha Jun Gu, Tao Xu, Qin-Hua Huang, Chu-Miao Zhang, Hai-Yan ChenDepartment of Health Check-Up Center, Jinshan Hospital, Fudan University, Shanghai 201508, Peoples Republic of ChinaBackground: Breast cancer is the most common malignant tumor that affects women with higher incidence. High-mobility group box 3 (HMGB3) plays critical functions in DNA repair, recombination, transcription and replication. This study aimed to investigate the effects of HMGB3 silence on mammosphere formation and tumor growth of breast cancer.Methods: LV5-HMGB3 and LV3-siHMGB3 vectors were transfected into MCF10A, MDA-MB-231, HCC1937, ZR-75-1 and MCF7 cells. Cell counting kit-8 (CCK-8) assay was used to evaluate cell proliferation. Xenograft tumor mice model was established by injection of MDA-MB-231. qRT-PCR and western blot were used to examine the expression of Nanog, Sox2 and OCT-4. Mammosphere forming
Mouse monoclonal HMGB1 antibody [HAP46.5] validated for WB, ELISA and tested in Human, Mouse and Rat. Referenced in 11 publications. Immunogen corresponding to…
ウサギ・ポリクローナル抗体 ab59463 交差種: Hu 適用: WB…HMGB1抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody 製品。国内在庫と品質保証制度も充実。
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Disease Markers is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies related to the identification of disease markers, the elucidation of their role and mechanism, as well as their application in the prognosis, diagnosis and treatment of diseases.
Endothelial inflammation plays an important role in hyperhomocysteinemia (HHcy)-associated vascular diseases. High mobility group box 1 (HMGB1) is a pro-inflammatory danger molecule produced by endothelial cells. However, whether HMGB1 is involved in vascular endothelial inflammation of HHcy is poorly understood. Neuropilin-1 (NRP1) mediates inflammatory response and activates mitogen-activated protein kinases (MAPKs) pathway that has been reported to be involved in regulation of HMGB1. The aim of this study was to determine the alteration of HMGB1 in HHcy, and the role of NRP1 in regulation of endothelial HMGB1 under high homocysteine (Hcy) condition. In the present study, we first observed that the plasma level of HMGB1 was elevated in HHcy patients and an experimental rat model, and increased HMGB1 was also observed in the thoracic aorta of an HHcy rat model. HMGB1 was induced by Hcy accompanied with upregulated NRP1 in vascular endothelial cells. Overexpression of NRP1 promoted expression ...
In various embodiments, the present invention is drawn to antibodies or antigen-binding fragments thereof that bind to a vertebrate high mobility group box (HMGB) polypeptide, methods of detecting and/or identifying an agent that binds to an HMGB polypeptide, methods of treating a condition in a subject characterized by activation of an inflammatory cytokine cascade and methods of detecting an HMGB polypeptide in a sample.
High-mobility group protein B1 (HMGB1) binds to the rs7903146 locus in the T-cell factor 7-like 2 (TCF7L2) gene in human pancreatic islets. / Zhou, Yuedan; Oskolkov, Nikolay; Shcherbina, Liliya; Ratti, Joyce; Kock, Kian-Hong; Su, Jing; Martin, Brian; Zackrisson Oskolkova, Malin; Göransson, Olga; Bacon, Julie; Li, Weimin; Bucciarelli, Saskia; Cilio, Corrado; Brazma, Alvis; Thatcher, Bradley; Rung, Johan; Wierup, Nils; Renström, Erik; Groop, Leif; Hansson, Ola.. In: Molecular and Cellular Endocrinology, Vol. 430, 15.07.2016, p. 138-145.. Research output: Research - peer-review › Journal article ...
Tör, Mahmut (2008) Pattern-recognition receptors [PRRs] in plants. In: 3rd International Damage Associated Molecular Pattern Molecules (DAMPs) and Alarmins Symposium, Pittsburgh, PA, Aug 30-Sep 02, 2008. Published in: Journal of Leukocyte Biology, Vol.84 (No.2). A1-A2. ...
Figure 2: LTX-315 induces immunogenic cell death in cancer cells. When treated with LTX-315, dying cancer cells release damage-associated molecular patterns (DAMP) such as calreticulin, ATP, HMGB1, mitochondria-derived DNA (mtDNA) and formyl peptides (FMIT). DAMPs bind to specific receptors on antigen-presenting cells such as dendritic cells (DC) and promotes their maturation and engulfment of tumor-antigens with subsequent presentation to T cells and execution of effective immune response (Zhou et al, and Eike et al, Oncotarget, 2015, Zhou et al, Cell Death and Disease, 2016, Sveinbjørnsson et al, Future Medicinal Chemistry, 2017) ...
Cell death is a key driver of disease progression and carcinogenesis in chronic liver disease (CLD), highlighted by the well-established clinical correlation between hepatocellular death and risk for the development of cirrhosis and hepatocellular carcinoma (HCC). Moreover, hepatocellular death is sufficient to trigger fibrosis and HCC in mice. However, the pathways through which cell death drives CLD progression remain elusive. Here, we tested the hypothesis that high-mobility group box 1 (HMGB1), a damage-associated molecular pattern (DAMP) with key roles in acute liver injury, may link cell death to injury responses and hepatocarcinogenesis in CLD. While liver-specific HMGB1 deficiency did not significantly affect chronic injury responses such as fibrosis, regeneration, and inflammation, it inhibited ductular/progenitor cell expansion and hepatocyte metaplasia. HMGB1 promoted ductular expansion independently of active secretion in a nonautonomous fashion, consistent with its role as a DAMP. ...
Cell death is a key driver of disease progression and carcinogenesis in chronic liver disease (CLD), highlighted by the well-established clinical correlation between hepatocellular death and risk for the development of cirrhosis and hepatocellular carcinoma (HCC). Moreover, hepatocellular death is sufficient to trigger fibrosis and HCC in mice. However, the pathways through which cell death drives CLD progression remain elusive. Here, we tested the hypothesis that high-mobility group box 1 (HMGB1), a damage-associated molecular pattern (DAMP) with key roles in acute liver injury, may link cell death to injury responses and hepatocarcinogenesis in CLD. While liver-specific HMGB1 deficiency did not significantly affect chronic injury responses such as fibrosis, regeneration, and inflammation, it inhibited ductular/progenitor cell expansion and hepatocyte metaplasia. HMGB1 promoted ductular expansion independently of active secretion in a nonautonomous fashion, consistent with its role as a DAMP. ...
A major discovery of recent decades has been the existence of stem cells and their potential to repair many, if not most, tissues. With the aging population, many attempts have been made to use exogenous stem cells to promote tissue repair, so far with limited success. An alternative approach, which may be more effective and far less costly, is to promote tissue regeneration by targeting endogenous stem cells. However, ways of enhancing endogenous stem cell function remain poorly defined. Injury leads to the release of danger signals which are known to modulate the immune response, but their role in stem cell-mediated repair in vivo remains to be clarified. Here we show that high mobility group box 1 (HMGB1) is released following fracture in both humans and mice, forms a heterocomplex with CXCL12, and acts via CXCR4 to accelerate skeletal, hematopoietic, and muscle regeneration in vivo. Pretreatment with HMGB1 2 wk before injury also accelerated tissue regeneration, indicating an acquired
Complete information for HMGB1P40 gene (Pseudogene), High Mobility Group Box 1 Pseudogene 40, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
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High mobility group box protein-1 promotes cerebral edema after traumatic brain injury via activation of toll-like receptor 4, 2014 ...
Among the most important findings of the present study is that pancreatic islets contain abundant HMGB1 compared with other organs and individual cell populations in the liver, the site of islet transplantation. Immunohistochemical staining of the pancreas revealed that HMGB1 is mainly stained in the nucleus of islet cells but not in other cell types, while HMGB1 is detected in the circulation after islet cell damage. In fact, the plasma concentration of HMGB1 in wild-type mice was elevated and peaked at 24 hours after i.v. injection of STZ and returned to the preinjection level 72 hours after STZ injection. The plasma levels of HMGB1 in diabetic recipient mice were elevated after islet transplantation with a peak at 6 hours and returned to pretransplant levels by 24 hours. These findings suggest that the first peak of the elevated HMGB1 levels is caused by destruction of islet cells by a toxic agent of STZ specific to β cells of islets and that the second peak in recipient mice after islet ...
cytoplasm, extracellular space, nuclear chromatin, nucleus, cis-regulatory region sequence-specific DNA binding, DNA binding, DNA binding, bending, double-stranded DNA binding, drug binding, four-way junction DNA binding