HMGB1 and its physiological and pathological roles

Naglova, H; Bucová, Mária

doi:10.4149/bll_2012_039

Cited by 56 publications

(59 citation statements)

References 128 publications

(128 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Taken together, these data represent a breakthrough in that Plasmodium HMGB2 is ascribed a major proinflammatory cytokine-like function reminiscent of that of its mammalian HMGB counterparts, which have been shown to play key roles in several human diseases, including sepsis, lupus, rheumatoid arthritis, and cancer (69).…”

Section: Discussionmentioning

confidence: 99%

Disruption of Parasitehmgb2Gene Attenuates Plasmodium berghei ANKA Pathogenicity

et al. 2015

View full text Add to dashboard Cite

h Eukaryotic high-mobility-group-box (HMGB) proteins are nuclear factors involved in chromatin remodeling and transcription regulation. When released into the extracellular milieu, HMGB1 acts as a proinflammatory cytokine that plays a central role in the pathogenesis of several immune-mediated inflammatory diseases. We found that the Plasmodium genome encodes two genuine HMGB factors, Plasmodium HMGB1 and HMGB2, that encompass, like their human counterparts, a proinflammatory domain. Given that these proteins are released from parasitized red blood cells, we then hypothesized that Plasmodium HMGB might contribute to the pathogenesis of experimental cerebral malaria (ECM), a lethal neuroinflammatory syndrome that develops in C57BL/6 (susceptible) mice infected with Plasmodium berghei ANKA and that in many aspects resembles human cerebral malaria elicited by P. falciparum infection. The pathogenesis of experimental cerebral malaria was suppressed in C57BL/6 mice infected with P. berghei ANKA lacking the hmgb2 gene (⌬hmgb2 ANKA), an effect associated with a reduction of histological brain lesions and with lower expression levels of several proinflammatory genes. The incidence of ECM in pbhmgb2-deficient mice was restored by the administration of recombinant PbHMGB2. Protection from experimental cerebral malaria in ⌬hmgb2 ANKA-infected mice was associated with reduced sequestration in the brain of CD4؉ and CD8 ؉ T cells, including CD8 ؉ granzyme B ؉ and CD8 ؉ IFN-␥ ؉ cells, and, to some extent, neutrophils. This was consistent with a reduced parasite sequestration in the brain, lungs, and spleen, though to a lesser extent than in wild-type P. berghei ANKA-infected mice. In summary, Plasmodium HMGB2 acts as an alarmin that contributes to the pathogenesis of cerebral malaria.

show abstract

Section: Discussionmentioning

confidence: 99%

Disruption of Parasitehmgb2Gene Attenuates Plasmodium berghei ANKA Pathogenicity

et al. 2015

View full text Add to dashboard Cite

show abstract

“…32,33) One of the local actions of extracellular HMGB1 is stimulation of tissue repair by recruiting stem cells and promotion of their proliferation. 11) With regard to the function of HMGB1 in tissue regeneration, Kitahara, et al reported that HMGB1 restores cardiac function through the activation of tissue angiogenesis after MI using male mice with a four-fold expression of HMGB1 in cardiac muscle cells (TG mice).…”

Section: Discussionmentioning

confidence: 99%

“…[5][6][7] HMGB1 secreted from necrotic cells into the extracellular space triggers tissue repair as a cytokine. [8][9][10][11] Moreover, several studies have proven that HMGB1 is involved in limiting the size of the infarct area and preserving cardiac function by promoting angiogenesis. 12,13) In addition, we have previously demonstrated that HMGB1 promotes angiogenesis and tissue repair by enhancing mobilization and differentiation of endothelial progenitor cells from bone marrow, resulting in preserving cardiac function after MI.…”

mentioning

confidence: 99%

DPP4 Inhibition Ameliorates Cardiac Function by Blocking the Cleavage of HMGB1 in Diabetic Mice After Myocardial Infarction

et al. 2017

View full text Add to dashboard Cite

SummaryHigh mobility group box 1 (HMGB1), a ubiquitous DNA-binding protein, promotes angiogenesis and tissue repair, resulting in restored cardiac function after myocardial infarction (MI). Although dipeptidyl peptidase 4 (DPP4) degrades certain peptides, it remains unclear as to whether HMGB1 is a substrate of DPP4 and whether DPP4 inhibition prevents the cleavage of HMGB1.In transgenic mice with cardiac-specific overexpression of HMGB1 (TG) and wild-type mice (WT), a diabetic state was induced by streptozotocin, and MI was created by ligation of the left anterior descending coronary artery. To inhibit DPP4 activity, a DPP4 inhibitor anagliptin was used. The plasma levels of HMGB1, infarct size, echocardiographic data, angiogenesis, and vascular endothelial growth factor (VEGF) expression in the peri-infarct area were compared among non-diabetic MI WT/TG, diabetic MI WT/TG, and anagliptin-treated diabetic MI WT/TG mice.DPP4 activity was increased in the diabetic state and blocked by anagliptin administration. The HMGB1 plasma levels were reduced in the diabetic TG compared with the non-diabetic TG mice, but DPP4 inhibition with anagliptin increased HMGB1 plasma levels in the diabetic TG mice. The infarct area was significantly larger in the diabetic TG than in the non-diabetic TG mice, and it was reduced by DPP4 inhibition. Cardiac function, angiogenesis, and VEGF expression were impaired in the diabetic TG mice, but they were ameliorated by the DPP4 inhibition to levels similar to those found in the non-diabetic TG mice.The DPP4 inhibitor ameliorated cardiac function by inhibiting the inactivation of HMGB1 in diabetic mice after MI.(Int Heart J 2017; 58: 778-786) Key words: Angiogenesis, Ischemic heart disease, Diabetes mellitus A cute myocardial infarction (MI) is an emergent disease caused by occlusion of the coronary artery. The morbidity and mortality of MI remain high despite the advancement of emergency medical services and the development of optimal therapies, including pharmacological treatment and percutaneous coronary intervention, and surgical technique. 1) Infarct size is known as an important prognostic predictor; thus, many studies of ischemic heart disease have been performed to determine how to limit the extent of infarction, focusing on the mechanisms of collateral development, ischemic reperfusion injury and ischemic preconditioning, among others. 2-4)High mobility group box 1 (HMGB1) is a ubiquitous non-histone DNA-binding protein that mediates gene transcription.5-7) HMGB1 secreted from necrotic cells into the extracellular space triggers tissue repair as a cytokine. [8][9][10][11] Moreover, several studies have proven that HMGB1 is involved in limiting the size of the infarct area and preserving cardiac function by promoting angiogenesis. 12,13) In addition, we have previously demonstrated that HMGB1 promotes angiogenesis and tissue repair by enhancing mobilization and differentiation of endothelial progenitor cells from bone marrow, resulting in preserving cardiac function after MI.14) Th...

show abstract

“…TLRs can attach many PAMPs/DAMPs and it is thought that they may even attach regular 'self-' molecules including fibrinogen and heat shock proteins, suggesting a relation between the stereotypic inflammatory response mediated through TLRs and autoimmune diseases [106,107]. The signaling of TLRs is transduced in the cytoplasm through the Toll/IL-1 receptor domain (TIR), which is the site for docking to the cytoplasmic adaptor proteins of TIR that are important in coordinating the pathways of signal transduction after TLR as well as IL-1 receptor activation.…”

Section: Gall Bladder Cancermentioning

confidence: 99%

Cancer and the microbiome: potential applications as new tumor biomarker

Khan

Gil-Bazo

Castiglia

et al. 2014

Expert Review of Anticancer Therapy

View full text Add to dashboard Cite

Authors contributed equallyMicrobial communities that colonize in humans are collectively described as microbiome. According to conservative estimates, about 15% of all types of neoplasms are related to different infective agents. However, current knowledge is not sufficient to explain how the microbiome contributes to the growth and development of cancers. Large and thorough studies involving colonized, diverse and complex microbiome entities are required to identify microbiome as a potential cancer marker and to understand how the immune system is involved in response to pathogens. This article reviews the existing evidence supporting the enigmatic association of transformed microbiome with the development of cancer through the immunological modification. Ascertaining the connection between microbiome and immunological responses with risk of cancer may direct to explaining significant advances in the etiology of cancer, potentially disclosing a novel paradigm of research for the management and prevention of cancer.

show abstract

HMGB1 and its physiological and pathological roles

Cited by 56 publications

References 128 publications

Disruption of Parasitehmgb2Gene Attenuates Plasmodium berghei ANKA Pathogenicity

Disruption of Parasitehmgb2Gene Attenuates Plasmodium berghei ANKA Pathogenicity

DPP4 Inhibition Ameliorates Cardiac Function by Blocking the Cleavage of HMGB1 in Diabetic Mice After Myocardial Infarction

Cancer and the microbiome: potential applications as new tumor biomarker

Contact Info

Product

Resources

About