HMGB proteins: Interactions with DNA and chromatin

Štros, Michal

doi:10.1016/j.bbagrm.2009.09.008

Cited by 534 publications

(569 citation statements)

References 190 publications

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“…High‐mobility group box 1 was initially identified as a nuclear protein that regulates various transcriptional factors to stabilize the nucleosome 21, while extracellular HMGB1, which can be either passively released from necrotic cells or actively secreted by activated inflammatory cells and stressed cells 8, 22, is reported to modulate inflammation through its high affinity receptors on the surface of target cells, including the receptor for advanced glycation end products and toll‐like receptors 2 and 4 23, 24. There exist growing recognition and experimental evidence to support that HMGB1 plays a pivotal role not only in the diseases such as sepsis, autoimmune disease, acute hepatic necrosis, acute lung injury 25, 26, 27, 28 but also in various heart diseases, including myocardial infarction and ischaemia‐reperfusion injury, however, with no consensus on the function of HMGB1 on the pathogenesis of the diseases 9, 16, 29, 30, 31, 32, 33, 34.…”

Section: Discussionmentioning

confidence: 99%

Extracellular high‐mobility group box 1 mediates pressure overload‐induced cardiac hypertrophy and heart failure

Zhang

Liu

Jiang

et al. 2015

J Cellular Molecular Medi

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Inflammation plays a key role in pressure overload‐induced cardiac hypertrophy and heart failure, but the mechanisms have not been fully elucidated. High‐mobility group box 1 (HMGB1), which is increased in myocardium under pressure overload, may be involved in pressure overload‐induced cardiac injury. The objectives of this study are to determine the role of HMGB1 in cardiac hypertrophy and cardiac dysfunction under pressure overload. Pressure overload was imposed on the heart of male wild‐type mice by transverse aortic constriction (TAC), while recombinant HMGB1, HMGB1 box A (a competitive antagonist of HMGB1) or PBS was injected into the LV wall. Moreover, cardiac myocytes were cultured and given sustained mechanical stress. Transthoracic echocardiography was performed after the operation and sections for histological analyses were generated from paraffin‐embedded hearts. Relevant proteins and genes were detected. Cardiac HMGB1 expression was increased after TAC, which was accompanied by its translocation from nucleus to both cytoplasm and intercellular space. Exogenous HMGB1 aggravated TAC‐induced cardiac hypertrophy and cardiac dysfunction, as demonstrated by echocardiographic analyses, histological analyses and foetal cardiac genes detection. Nevertheless, the aforementioned pathological change induced by TAC could partially be reversed by HMGB1 inhibition. Consistent with the in vivo observations, mechanical stress evoked the release and synthesis of HMGB1 in cultured cardiac myocytes. This study indicates that the activated and up‐regulated HMGB1 in myocardium, which might partially be derived from cardiac myocytes under pressure overload, may be of crucial importance in pressure overload‐induced cardiac hypertrophy and cardiac dysfunction.

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Section: Discussionmentioning

confidence: 99%

Extracellular high‐mobility group box 1 mediates pressure overload‐induced cardiac hypertrophy and heart failure

Zhang

Liu

Jiang

et al. 2015

J Cellular Molecular Medi

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“…During necrosis, the acidic tail is modified by poly(ADP)-ribosylation, which is required for relocation of HMGB1 from the nucleus to cytoplasm. 1 In Arabidopsis (Arabidopsis thaliana), the C-terminal acidic domain is critical for the localization of HMGB2 and HMGB4 in the cytoplasm. 48 After GCRV challenge, the ratio of nuclear export of CiHMGB2bN1box, 2N3C and 3N2C was significantly lower than that of CiHMGB2b.…”

Section: Discussionmentioning

confidence: 99%

“…In mammals, there are four family members (HMGB1-4), of which HMGB1, 2 and 3 are characterized by two DNA-binding domains (HMG-box A and B) and a Cterminal acidic tail domain and HMGB4 possesses two HMG-boxes but lacks the acidic tail. 1 In some teleosts, such as fugu (Takifugu), medaka (Oryzias latipes), Tetraodon and stickleback, two paralogous genes were detected for HMGB1 and HMGB2 but not for HMGB3. 2 However, in zebrafish (Danio rerio), salmon (Oncorhynchus), carp (Cyprinus carpio) 2 and grass carp (Ctenopharyngodon idella), [3][4][5] two paralogs are present within each of the HMGB subfamilies (HMGB1, HMGB2, HMGB3).…”

Section: Introductionmentioning

confidence: 99%

“…Traditionally serving as architectural factors of chromatin, HMGBs play pivotal roles in transcriptional regulation, DNA repair, recombination, differentiation, extracellular signaling and nucleosome remodeling. 1,6 Recent discoveries illustrate that HMGBs, particularly HMGB1, function as cytokines or pro-inflammatory factors, playing a pivotal role in crosslinking innate and adaptive immunity. [7][8][9] Various studies have also highlighted the novel feature of HMGBs that function as universal sentinels for nucleic-acid-mediated innate immune responses.…”

Section: Introductionmentioning

confidence: 99%

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Dynamic localization and the associated translocation mechanism of HMGBs in response to GCRV challenge in CIK cells

Rao

Yang

et al. 2014

Cell Mol Immunol

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High-mobility group box (HMGB) proteins, a family of chromatin-associated nuclear proteins, play amazingly multifaceted roles in the immune system of mammals. Thus far, little is known about the nucleocytoplasmic distribution of HMGBs in teleosts. The present study systematically investigated the dynamic localization of all six HMGB proteins in Ctenopharyngodon idella kidney (CIK) cells. Under basal conditions, all HMGBs exclusively localized to the nucleus. Grass carp reovirus (GCRV), polyinosinic-polycytidylic (poly(I : C)) potassium salt and lipopolysaccharide (LPS) challenge evoked the nuclear export of HMGBs to various degrees: GCRV challenge induced the highest nuclear export of CiHMGB2b, and poly(I : C) and LPS evoked the highest nucleocytoplasmic shuttling of CiHMGB1b. Overall, the nucleocytoplasmic shuttling of CiHMGB2a and CiHMGB3b was rarely induced by these challenges. Dynamic imaging uncovered that the nucleocytoplasmic GCRV-induced relocation of CiHMGB2b occurred in cells undergoing karyotheca rupture, apoptosis or proliferation. Western blot analyses were used to examine HMGB-EGFP fusion proteins in whole cell lysates, cytosol, nuclear fractions and culture medium. Further investigation demonstrated the nuclear retention of N-terminal HMG-boxes and the nucleocytoplasmic distribution of the C-terminal acidic tails. Comparative analyses of the dynamic relocation of full-length, truncated or chimeric HMGBs confirmed that the intramolecular interaction between HMG-boxes and C-tail domains mediated the nucleocytoplasmic translocation of HMGBs. These results not only provide an overall understanding of the subcellular localization of HMGBs, but also reveal the induction mechanism of the nucleocytoplasmic translocation of HMGBs by GCRV challenge, which lays a foundation for further studies on the interactions among pathogens, HMGBs and pattern recognition receptors in the innate immunity of teleosts. Keywords: grass carp (Ctenopharyngodon idella); grass carp reovirus; HMGBs; innate immunity; subcellular localization INTRODUCTION High-mobility group box (HMGB) proteins are abundant non-histone chromatin components implicated in major DNA transactions. In mammals, there are four family members (HMGB1-4), of which HMGB1, 2 and 3 are characterized by two DNA-binding domains (HMG-box A and B) and a Cterminal acidic tail domain and HMGB4 possesses two HMG-boxes but lacks the acidic tail. 1 In some teleosts, such as fugu (Takifugu), medaka (Oryzias latipes), Tetraodon and stickleback, two paralogous genes were detected for HMGB1 and HMGB2 but not for HMGB3. 2 However, in zebrafish (Danio rerio), salmon (Oncorhynchus), carp (Cyprinus carpio) 2 and grass carp (Ctenopharyngodon idella), 3-5 two paralogs are present within each of the HMGB subfamilies (HMGB1,

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“…22 It can be actively secreted by monocytes/macrophages, DC and other cells in response to pathogen-derived, pro-inflammatory or stress signals. [23][24][25] Moreover, HMGB1 is a prototypic damageassociated molecular pattern passively released from necrotic cells.…”

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confidence: 99%

Necrotic cell-derived high mobility group box 1 attracts antigen-presenting cells but inhibits hepatocyte growth factor-mediated tropism of mesenchymal stem cells for apoptotic cell death

et al. 2015

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Tissue damage due to apoptotic or necrotic cell death typically initiates distinct cellular responses, leading either directly to tissue repair and regeneration or to immunological processes first, to clear the site, for example, of potentially damage-inducing agents. Mesenchymal stem cells (MSC) as well as immature dendritic cells (iDC) and monocytes migrate to injured tissues. MSC have regenerative capacity, whereas monocytes and iDC have a critical role in inflammation and induction of immune responses, including autoimmunity after tissue damage. Here, we investigated the influence of apoptotic and necrotic cell death on recruitment of MSC, monocytes and iDC, and identified hepatocyte growth factor (HGF) and the alarmin high mobility group box 1 (HMGB1) as key factors differentially regulating these migratory responses. MSC, but not monocytes or iDC, were attracted by apoptotic cardiomyocytic and neuronal cells, whereas necrosis induced migration of monocytes and iDC, but not of MSC. Only apoptotic cell death resulted in HGF production and HGF-mediated migration of MSC towards the apoptotic targets. In contrast, HMGB1 was predominantly released by the necrotic cells and mediated recruitment of monocytes and iDC via the receptor of advanced glycation end products. Moreover, necrotic cardiomyocytic and neuronal cells caused an HMGB1/toll-like receptor-4-dependent inhibition of MSC migration towards apoptosis or HGF, while recruitment of monocytes and iDC by necrosis or HMGB1 was not affected by apoptotic cells or HGF. Thus, the type of cell death differentially regulates recruitment of either MSC or monocytes and iDC through HGF and HMGB1, respectively, with a dominant, HMGB1-mediated role of necrosis in determining tropism after tissue injury.

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HMGB proteins: Interactions with DNA and chromatin

Cited by 534 publications

References 190 publications

Extracellular high‐mobility group box 1 mediates pressure overload‐induced cardiac hypertrophy and heart failure

Extracellular high‐mobility group box 1 mediates pressure overload‐induced cardiac hypertrophy and heart failure

Dynamic localization and the associated translocation mechanism of HMGBs in response to GCRV challenge in CIK cells

Necrotic cell-derived high mobility group box 1 attracts antigen-presenting cells but inhibits hepatocyte growth factor-mediated tropism of mesenchymal stem cells for apoptotic cell death

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