Role of high mobility group protein-1 (HMG1) in amyloid-β homeostasis

Takata, Kazuyuki; Kitamura, Yoshihisa; Kakimura, Jun Ichi; Shibagaki, Keiichi; Tsuchiya, Daiju; Taniguchi, Takashi; Smith, Mark A.; Perry, George; Shimohama, Shun

doi:10.1016/s0006-291x(03)00024-x

Cited by 80 publications

(70 citation statements)

References 18 publications

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“…TLR4 binding as well as cotrafficking properties and roles in the initiation of an immune response have been assigned also to hsp22, hsp70, hsp72, hsp90, gp96 (hsp90b1), chlamydial hsp60, and Francisella tularensis hsp DnaK (24,26,43,251,470,793,925,926). Similarly, the high-mobility group box 1 protein (HMGB1, HMG1, amphoterin) was found to inhibit amyloid ␤ uptake (891) and to amplify inflammatory responses in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (18). A direct link of neurodegenerative processes in AD to microglial TLR4 became obvious when amyloid ␤ fibrilles were found to bind to CD14, the prominent coreceptor for LPS signaling via TLR4 (270).…”

Section: A Toll-like Receptorsmentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,090

2,981

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Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

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Section: A Toll-like Receptorsmentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,090

2,981

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“…As a cytokine-like factor, HMGB1 is secreted by macrophages, mature dendritic cells and natural killer cells in response to injury, infection, or other inflammatory stimuli [3,4]. The biological importance of HMGB1 is underscored by its multifunctionality, as well as pathologic conditions caused in a man by its deregulation: Alzheimer's Disease [5], arthritis [6], and cancer [7]. HMGB1 release into the extracellular environment is mediated by active and passive mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Serum levels of HMGB1, survivin, and VEGF in patients with advanced non-small cell lung cancer during chemotherapy.

Naumnik

Nilklińska²,

Ossolińska³

et al. 2010

Folia Histochem Cytobiol.

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Abstract:Recently, several reports have suggested that HMGB1 (the high-mobility group box-1) plays a key role in tumor angiogenesis through multiple mechanisms, including up-regulation of proangiogenic factors. This study was conducted to investigate the prognostic role and the effects of chemotherapy on serum (ELISA) angiogenic factors: HMGB1, survivin and VEGF (Vascular Endothelial Growth Factor) in patients with advanced stage non-small cell lung cancer (NSCLC). The study entered 40 patients (31 man) and 15 healthy volunteers (control group). Peripheral blood samples were taken before and after four cycles of chemotherapy. The mean serum HMGB1 and VEGF levels were significantly higher in patients with advanced NSCLC than in controls (p=0.024, p=0.028, respectively). The levels of survivin in NSCLC patients were comparable to controls. No correlation was found between HMGB1, survivin and VEGF concentrations and the histological type and staging of lung cancer. Similarly, no correlation was revealed between the concentrations of HMGB1, survivin and VEGF and the effect of chemotherapy. However, in patients with NSCLC, HMGB1 positevely correlated with survivin (R=0.814, p=0.007) before chemotherapy, and negatively with VEGF (R=-0.841, p=0.035) after chemotherapy. When the cut-off values of serum HMGB1, survivin and VEGF (2.38 ng/ml, 81.92 pg/ml, 443.26 pg/ml, respectively) were used, the prognoses of high and low groups were not different. Concluding, patients with NSCLC have a higher serum concentration of HMGB1 and VEGF, while survivin levels are comparable to healthy individuals. In our opinion, determination of HMGB1, survivin and VEGF concentrations has no clinical significance in the prognosis of the survival time in lung cancer.

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“…The local extracellular accumulation of this cytokine in the brain, as a result of its intracerebroventricular administration or its release from dying neurons during cerebral ischemia, elicits local inflammatory events in mice (8 -10). Moreover, HMGB1 also promotes neuroinflammation in postischemic rat brain (9) and in the neurodegenerative processes associated to Alzheimer's disease (11,12). Hence, new information on the role of single phenotypes in the brain's responses to extracellular HMGB1 is of crucial value with regard to possible therapeutic applications.…”

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confidence: 99%

Selective Proinflammatory Activation of Astrocytes by High-Mobility Group Box 1 Protein Signaling

Pedrazzi

Patrone

Passalacqua

et al. 2007

The Journal of Immunology

117

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Extracellular high-mobility group box 1 protein (HMGB1) triggers inflammatory events in the brain. We demonstrate that astrocytes, the main glial cells in the brain, acquire a specific reactive phenotype when exposed to HMGB1. This cell activation, which involves the receptor for advanced glycation end-products and the MAPK/ERK1/2 cascade, results in the transcriptional/translational induction of a restricted number of inflammatory mediators, including cyclooxygenase-2, matrix metalloproteinase-9, and several chemokines of the CC and CXC families. The mixture of factors released by HMGB1-reactive astrocytes displays a potent chemotactic activity on human monocytic cells. This study is the first to suggest that HMGB1/astrocyte interaction plays a specific functional role in the progression of inflammatory processes in the CNS by facilitating local leukocyte infiltration.

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Role of high mobility group protein-1 (HMG1) in amyloid-β homeostasis

Cited by 80 publications

References 18 publications

Physiology of Microglia

Physiology of Microglia

Serum levels of HMGB1, survivin, and VEGF in patients with advanced non-small cell lung cancer during chemotherapy.

Selective Proinflammatory Activation of Astrocytes by High-Mobility Group Box 1 Protein Signaling

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