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  • 99
    Thermo Fisher hmgb 1
    Hmgb 1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore anti hmg b1
    Anti Hmg B1, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc hmgb 1
    Hmgb 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti hmgb 1
    Effect of Exc-B on MAPK, HO-1, and <t>HMGB-1</t> in homogenized knee synovial tissues. Western blot analysis of the effects of subcutaneous Exc-B administration on protein expression of HO-1, HMGB-1, and MAPK signalling, as well as GAPDH in knee synovial tissue homogenates from rats with: AIA ( A ); or CIA ( B ). Exc-B (2.5 or 5 mg/kg) significantly inhibits HMGB-1 and MAPK signalling and upregulates HO-1 protein expression after immunization. The There is no difference between groups in the protein expression of GAPDH in synovial tissues. Quantification values reflect the mean ± S.E.M. of three different experiments. n = 6 rat per group. The data were analysed by one-way analysis of variance (ANOVA) followed by the Student–Newman–Keuls post hoc test. * p
    Anti Hmgb 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam anti hmg b1
    Glia mediates the effect of <t>HMGB-1.</t> ( A ) Primary pericytes co-cultured with glia were treated with HMGB-1 (5 µg/mL, 24 hours). Pericyte survival was assessed using an apoptosis assay kit. All experiments were repeated at least three times (**P
    Anti Hmg B1, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam hmgb 1
    RAGE binding of S100P, S100A4, and <t>HMGB-1</t> was inhibited by an S100P-derived RAGE antagonistic peptide (RAP)
    Hmgb 1, supplied by Abcam, used in various techniques. Bioz Stars score: 93/100, based on 222 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    HMGBiotech hmgb 1
    <t>HMGB-1–induced</t> changes in the expression of SVEC surface adhesion molecules. (A) Representative immunofluorescent staining of β1-integrin in untreated and TNF-α, SDF-1α or HMGB-1–treated SVEC. (B) Number of SVEC showing β1-integrin polarization within the groups. (C) Representative images of P-selectin expression on SVEC plasmalemma in untreated and TNF-α, SDF-1α or HMGB-1–treated cells. (D) Number of SVEC showing P-selectin redistribution after stimulation with different cytokines. (E) Confocal images of ICAM-1 expression patterns on SVEC membrane. (F) Quantity of cells presenting ICAM-1 polarization after preconditioning with TNF-α, SDF-1α or HMGB-1 (* P
    Hmgb 1, supplied by HMGBiotech, used in various techniques. Bioz Stars score: 92/100, based on 1018 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Shino-Test Corporation hmgb 1
    Effects of extracorporeal blood purification (EBP) on high-mobility group box 1 <t>(HMGB-1)</t> Plasma HMGB-1 levels are shown over time (mean ± s.e.m., ng/ml). * P
    Hmgb 1, supplied by Shino-Test Corporation, used in various techniques. Bioz Stars score: 93/100, based on 69 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abnova hmgb 1
    Reduced expression of proinflammatory factors in mesenchymal stem cells (MSCs) overexpressing the soluble receptor for advanced glycation end products(sRAGE). ( A ) Schematic representation of sRAGE DNA vector constructs. ( B ) MSCs were transfected with mock or sRAGE vector using the X-tremeGENE HP reagent for 3 days. RAGE and high-mobility group box-1 <t>(HMGB-1)</t> levels in MSCs and sRAGE-MSCs were measured by ELISA and western blotting. ( C ) Transcript levels of vascular endothelial growth factor ( VEGF ), interleukin-1β ( IL-1β ), IL-6 , HMGB-1 , IL-10 , transforming growth factor-β ( TGF-β ), indoleamine 2,3-dioxygenase ( IDO ), and hepatocyte growth factor ( HGF ) were determined using real-time PCR. Data represent the mean ± s.d. (bar) values from three independent experiments. * P
    Hmgb 1, supplied by Abnova, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Becton Dickinson hmgb 1
    In vitro characterization of the different cell death modalities induced in CT26 cells. (A) FACS analysis of cells treated in vitro with the indicated agents as specified in Materials and methods. ZVAD, Z-VAD-fmk. Numbers indicate the percentage of cells (X ± SD, n = 5) in each quadrant. (B) Immunoblot analyses of cells treated as in A. Cellular extracts were subjected to the immunodetection of activated caspase 3 (Casp3a), <t>HMGB-1,</t> and HSP-70. (C) TUNEL staining (green) of cells counterstained with DAPI (blue). The percentage of TUNEL + cells (X ± SEM, n = 3) was determined. (D) Transmission electron microscopy. Representative microphotographs are shown. Apoptotic cells showing chromatin condensation are labeled with an “A.” (E) Cells treated with the indicated agents as in A were washed and plated to determine the frequency of surviving clones, defining the control value of untreated cells as 100%. Results are representative of three independent experiments.
    Hmgb 1, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 92/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Elabscience hmgb 1
    In vitro characterization of the different cell death modalities induced in CT26 cells. (A) FACS analysis of cells treated in vitro with the indicated agents as specified in Materials and methods. ZVAD, Z-VAD-fmk. Numbers indicate the percentage of cells (X ± SD, n = 5) in each quadrant. (B) Immunoblot analyses of cells treated as in A. Cellular extracts were subjected to the immunodetection of activated caspase 3 (Casp3a), <t>HMGB-1,</t> and HSP-70. (C) TUNEL staining (green) of cells counterstained with DAPI (blue). The percentage of TUNEL + cells (X ± SEM, n = 3) was determined. (D) Transmission electron microscopy. Representative microphotographs are shown. Apoptotic cells showing chromatin condensation are labeled with an “A.” (E) Cells treated with the indicated agents as in A were washed and plated to determine the frequency of surviving clones, defining the control value of untreated cells as 100%. Results are representative of three independent experiments.
    Hmgb 1, supplied by Elabscience, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Tecan Systems hmgb 1
    ( A ) Rate of early allograft dysfunction (EAD) with effluent above <t>HMGB-1</t> and below 580 ng/ml. With HMGB-1 values above 580 ng/ml, only 1 out of 13 patients did not develop EAD. ( B ) Rate of initial non-function (INF) with effluent HMGB-1 above and below 1608 ng/ml. With HMGB-1 values below 1608 ng/ml, only 1 out of 26 patients developed INF.
    Hmgb 1, supplied by Tecan Systems, used in various techniques. Bioz Stars score: 92/100, based on 64 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    USCN Life hmgb 1
    Plasma CTRP-3 (a) and <t>HMGB-1</t> (b) concentrations in different subgroups and in males and females ((c) and (d)). Data were presented as means ± standard deviation. Differences between multiple groups were tested by analysis of variance (ANOVA) for continuous variables. P for trend was estimated by a linear-by-linear association of the chi-square test. ∗ P
    Hmgb 1, supplied by USCN Life, used in various techniques. Bioz Stars score: 90/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Chondrex inc hmgb 1
    Elimination of RAGE does not influence remote organ (liver) injury and systemic inflammation following intestinal IR . Mice were subjected to 30 min mesenteric artery occlusion, followed by 150 min reperfusion. Peripheral blood samples were collected from WT-SHAM, WT-IR, and RAGE −/− IR groups for enzyme activity and pro-inflammatory markers. (A,B) Activities of liver enzymes ALT (A) and ALP (B) measured as markers of liver injury. (C,D) Levels of pro-inflammatory mediators <t>HMGB-1</t> (C) and IL-6 (D) . Data are presented as mean ± SEM, n = 5 (WT-SHAM); n = 13 (WT-IR); n = 15 (RAGE −/− IR) where * p
    Hmgb 1, supplied by Chondrex inc, used in various techniques. Bioz Stars score: 92/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Lifespan Biosciences hmgb 1
    Elimination of RAGE does not influence remote organ (liver) injury and systemic inflammation following intestinal IR . Mice were subjected to 30 min mesenteric artery occlusion, followed by 150 min reperfusion. Peripheral blood samples were collected from WT-SHAM, WT-IR, and RAGE −/− IR groups for enzyme activity and pro-inflammatory markers. (A,B) Activities of liver enzymes ALT (A) and ALP (B) measured as markers of liver injury. (C,D) Levels of pro-inflammatory mediators <t>HMGB-1</t> (C) and IL-6 (D) . Data are presented as mean ± SEM, n = 5 (WT-SHAM); n = 13 (WT-IR); n = 15 (RAGE −/− IR) where * p
    Hmgb 1, supplied by Lifespan Biosciences, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam hmgb 1 antibody
    SP-A interaction with Mp-stimulated DCs Bone marrow derived dendritic cells were cultured for 6 days in the presence of GM-CSF, purified and stimulated with Mp (10 cfu/cell) for 16 hours in the presence or absence of SP-A (50 μg/ml). Supernatants and lysates were harvested for analysis by SDS-PAGE and western immunoblotting for either <t>HMGB-1,</t> SP A or GAPDH. A , immature dendritic cells were used immediately after purification on day 6 or B , mature dendritic cells were stimulated for 24 hours in the presence of LPS prior to studies with Mp. C , dendritic cells were either treated for 16 hours with nothing (lane 1), pre-incubated with SP-A, washed, then stimulated with media (lane 2) or Mp (lane 3), or stimulated with SP-A coated Mp (lane 4) or non-coated Mp (lane 5). D , dendritic cells were pre-incubated with a TLR-2 neutralizing antibody or isotype control antibody prior to stimulation with Mp for 16 hours. Blots are representative from experiments conducted from 3 independent BMDC cultures.
    Hmgb 1 Antibody, supplied by Abcam, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore hmgb 1
    The damage-associated molecules, <t>HMGB-1</t> and ATP induce expression of IL-33 mRNA in sinonasal epithelial cells derived from recalcitrant CRSwNP subjects. Data is expressed as fold increase over unstimulated condition within individual subjects. * p= 0.046; **p=0.033
    Hmgb 1, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 103 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems hmgb 1
    TAK-242 inhibits both LPS-induced and <t>HMGB-1-induced</t> TNF-α production in RAW264.7 cells. Cells were cultured with 0.5 ng·mL −1 LPS or 10 µg·mL −1 HMGB-1 for 20 h in the presence of 0.1 ng·mL −1
    Hmgb 1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 99/100, based on 44 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Shanghai GenePharma sirna hmgb 1 transfection sirna hmgb 1
    <t>SiRNA</t> <t>HMGB-1</t> effect on TLR4 and NF-κB mRNA expression in RGC-5. ( A ) SiRNA HMGB-1 effect on TLR4 mRNA expression in RGC-5; ( B ) SiRNA HMGB-1 effect on NF-κB mRNA expression in RGC-5.* TLR-4 P=0.009; NF-κB P=0.017, compared with control; # TLR-4 P=0.033; NF-κB P=0.024, compared with high glucose group.
    Sirna Hmgb 1 Transfection Sirna Hmgb 1, supplied by Shanghai GenePharma, used in various techniques. Bioz Stars score: 88/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Effect of Exc-B on MAPK, HO-1, and HMGB-1 in homogenized knee synovial tissues. Western blot analysis of the effects of subcutaneous Exc-B administration on protein expression of HO-1, HMGB-1, and MAPK signalling, as well as GAPDH in knee synovial tissue homogenates from rats with: AIA ( A ); or CIA ( B ). Exc-B (2.5 or 5 mg/kg) significantly inhibits HMGB-1 and MAPK signalling and upregulates HO-1 protein expression after immunization. The There is no difference between groups in the protein expression of GAPDH in synovial tissues. Quantification values reflect the mean ± S.E.M. of three different experiments. n = 6 rat per group. The data were analysed by one-way analysis of variance (ANOVA) followed by the Student–Newman–Keuls post hoc test. * p

    Journal: Marine Drugs

    Article Title: Excavatolide B Attenuates Rheumatoid Arthritis through the Inhibition of Osteoclastogenesis

    doi: 10.3390/md15010009

    Figure Lengend Snippet: Effect of Exc-B on MAPK, HO-1, and HMGB-1 in homogenized knee synovial tissues. Western blot analysis of the effects of subcutaneous Exc-B administration on protein expression of HO-1, HMGB-1, and MAPK signalling, as well as GAPDH in knee synovial tissue homogenates from rats with: AIA ( A ); or CIA ( B ). Exc-B (2.5 or 5 mg/kg) significantly inhibits HMGB-1 and MAPK signalling and upregulates HO-1 protein expression after immunization. The There is no difference between groups in the protein expression of GAPDH in synovial tissues. Quantification values reflect the mean ± S.E.M. of three different experiments. n = 6 rat per group. The data were analysed by one-way analysis of variance (ANOVA) followed by the Student–Newman–Keuls post hoc test. * p

    Article Snippet: Membranes were blocked for 60 min at room temperature with 5% non-fat dry milk in Tris-buffered saline with Tween 20 (TTBS; 0.1% Tween 20, 20 mM Tris–HCl, pH 7.4, 137 mM NaCl) and then incubated overnight at 4 °C with primary antibodies against anti-HO-1 (1:1000; Enzo Life Sciences, Farmingdale, NY, USA; catalogue no. ADI-SPA-895), anti-HMGB-1 (1:1000; Cell Signaling Technology Inc., Danvers, MA, USA; catalogue no. 3935), anti-p-ERK (1:1000; Cell Signaling Technology Inc.; catalogue no. 9102), anti-ERK (1:1000; Gene Tex Inc., Irvine, CA, USA; catalogue no. gtx627408), anti-p-JNK (1:1000; Cell Signaling Technology Inc.; catalogue no. 4668), anti-JNK (1:1000; Cell Signaling Technology Inc.; catalogue no. 9252), anti-p-P38 (1:1000; Cell Signaling Technology Inc.; catalogue no. 4511), anti-P38 (1:1000; Cell Signaling Technology Inc.; catalogue no. 9212), and GAPDH (1:1000; Gene Tex Inc.; catalogue no. gtx627408).

    Techniques: Western Blot, Expressing

    Glia mediates the effect of HMGB-1. ( A ) Primary pericytes co-cultured with glia were treated with HMGB-1 (5 µg/mL, 24 hours). Pericyte survival was assessed using an apoptosis assay kit. All experiments were repeated at least three times (**P

    Journal: PLoS ONE

    Article Title: Cellular Mechanisms of High Mobility Group 1 (HMGB-1) Protein Action in the Diabetic Retinopathy

    doi: 10.1371/journal.pone.0087574

    Figure Lengend Snippet: Glia mediates the effect of HMGB-1. ( A ) Primary pericytes co-cultured with glia were treated with HMGB-1 (5 µg/mL, 24 hours). Pericyte survival was assessed using an apoptosis assay kit. All experiments were repeated at least three times (**P

    Article Snippet: Proteins were blotted onto a PVDF membrane (Invitrogen, Carlsbad, CA) and incubated with HMGB-1 primary antibody (1∶1000, Abcam, Cambridge, MA).

    Techniques: Cell Culture, Apoptosis Assay

    HMGB-1 can affect retinal endothelial cell activity. ( A ) Expression of CCL2 and CCL5 chemokines, IL-1β and IL-6 cytokines, as well as cell adhesion molecule ICAM-1 in HMGB-1-treated (5 and 10 µg/ml) and control (PBS-treated) retinal endothelial cells. Gene expression was assessed using quantitative RT-PCR in cells exposed to HMGB-1 or PBS after 24 hours (*P

    Journal: PLoS ONE

    Article Title: Cellular Mechanisms of High Mobility Group 1 (HMGB-1) Protein Action in the Diabetic Retinopathy

    doi: 10.1371/journal.pone.0087574

    Figure Lengend Snippet: HMGB-1 can affect retinal endothelial cell activity. ( A ) Expression of CCL2 and CCL5 chemokines, IL-1β and IL-6 cytokines, as well as cell adhesion molecule ICAM-1 in HMGB-1-treated (5 and 10 µg/ml) and control (PBS-treated) retinal endothelial cells. Gene expression was assessed using quantitative RT-PCR in cells exposed to HMGB-1 or PBS after 24 hours (*P

    Article Snippet: Proteins were blotted onto a PVDF membrane (Invitrogen, Carlsbad, CA) and incubated with HMGB-1 primary antibody (1∶1000, Abcam, Cambridge, MA).

    Techniques: Activity Assay, Expressing, Quantitative RT-PCR

    HMGB-1 induces expression of pro-inflammatory markers in astrocytes (A) and microglial cells (B) isolated from wild type (WT) animals. TLR4 deficiency (Tlr4KO) suppresses induction of pro-inflammatory markers after HMGB-1 treatment. Gene expression was assessed using quantitative RT-PCR in PBS treated controls and HMGB-1 treated cells. For each gene, results are expressed as a percentage of the corresponding value in the PBS treated primary glial cell cultures isolated from WT animals after normalization to β-actin (*P

    Journal: PLoS ONE

    Article Title: Cellular Mechanisms of High Mobility Group 1 (HMGB-1) Protein Action in the Diabetic Retinopathy

    doi: 10.1371/journal.pone.0087574

    Figure Lengend Snippet: HMGB-1 induces expression of pro-inflammatory markers in astrocytes (A) and microglial cells (B) isolated from wild type (WT) animals. TLR4 deficiency (Tlr4KO) suppresses induction of pro-inflammatory markers after HMGB-1 treatment. Gene expression was assessed using quantitative RT-PCR in PBS treated controls and HMGB-1 treated cells. For each gene, results are expressed as a percentage of the corresponding value in the PBS treated primary glial cell cultures isolated from WT animals after normalization to β-actin (*P

    Article Snippet: Proteins were blotted onto a PVDF membrane (Invitrogen, Carlsbad, CA) and incubated with HMGB-1 primary antibody (1∶1000, Abcam, Cambridge, MA).

    Techniques: Expressing, Isolation, Quantitative RT-PCR

    HMGB-1 directly mediates retinal endothelial cell death. ( A ) Expression of HMGB-1 receptors (TLR4 and RAGE) in HMGB-1-treated (5 and 10 µg/ml) and control (PBS-treated) retinal endothelial cells. ( B ) Treatment with HMGB-1 (10 µg/ml) increases cell death in primary human retinal endothelial cell cultures. All experiments were repeated at least three times (*P

    Journal: PLoS ONE

    Article Title: Cellular Mechanisms of High Mobility Group 1 (HMGB-1) Protein Action in the Diabetic Retinopathy

    doi: 10.1371/journal.pone.0087574

    Figure Lengend Snippet: HMGB-1 directly mediates retinal endothelial cell death. ( A ) Expression of HMGB-1 receptors (TLR4 and RAGE) in HMGB-1-treated (5 and 10 µg/ml) and control (PBS-treated) retinal endothelial cells. ( B ) Treatment with HMGB-1 (10 µg/ml) increases cell death in primary human retinal endothelial cell cultures. All experiments were repeated at least three times (*P

    Article Snippet: Proteins were blotted onto a PVDF membrane (Invitrogen, Carlsbad, CA) and incubated with HMGB-1 primary antibody (1∶1000, Abcam, Cambridge, MA).

    Techniques: Expressing

    HMGB-1 does not directly mediate pericyte death. ( A ) Treatment with HMGB-1 (10 µg/ml) does not increase cell death in pure primary human pericyte cultures. All experiments were repeated at least three times. ( B ) Pericyte death was determined using annexin V as a marker of apoptotic cells and annexinV/propidium iodide (PI) to identify necrotic cells.

    Journal: PLoS ONE

    Article Title: Cellular Mechanisms of High Mobility Group 1 (HMGB-1) Protein Action in the Diabetic Retinopathy

    doi: 10.1371/journal.pone.0087574

    Figure Lengend Snippet: HMGB-1 does not directly mediate pericyte death. ( A ) Treatment with HMGB-1 (10 µg/ml) does not increase cell death in pure primary human pericyte cultures. All experiments were repeated at least three times. ( B ) Pericyte death was determined using annexin V as a marker of apoptotic cells and annexinV/propidium iodide (PI) to identify necrotic cells.

    Article Snippet: Proteins were blotted onto a PVDF membrane (Invitrogen, Carlsbad, CA) and incubated with HMGB-1 primary antibody (1∶1000, Abcam, Cambridge, MA).

    Techniques: Marker

    There was no association found between the level of HMGB-1 and neovascularization in the retina. Neovascularization was induced by subretinally injecting Matrigel either with PBS ( A ) or mixed with HMGB-1 ( B ). Neovascularization was allowed to develop for 10 days. Blood vessels were labeled with DiI and visualized by fluorescence microscopy (white arrows indicate neovascularization in the Matrigel injected area. Ch, choroids; M, Matrigel, R retina. Scale bar: 200 µm). ( C ) Quantitative analysis shows no difference in the levels of neovascularization between HMGB1-treated eyes compared to control eyes. ( D ) VEGF-A expression was not changed in glial cells (astrocytea and microglia) treated with HMGB-1 and PBS (control). ( E ) Examination by western blot of vitreous humor from both hyperoxia-injured and room air control animals (obtained from postnatal days 15 and 17 pups) did not show a statistically significant difference between them. Results of analysis of western blots (top) are expressed as a percentage of corresponding value in the control eyes ± SEM (n = 6).

    Journal: PLoS ONE

    Article Title: Cellular Mechanisms of High Mobility Group 1 (HMGB-1) Protein Action in the Diabetic Retinopathy

    doi: 10.1371/journal.pone.0087574

    Figure Lengend Snippet: There was no association found between the level of HMGB-1 and neovascularization in the retina. Neovascularization was induced by subretinally injecting Matrigel either with PBS ( A ) or mixed with HMGB-1 ( B ). Neovascularization was allowed to develop for 10 days. Blood vessels were labeled with DiI and visualized by fluorescence microscopy (white arrows indicate neovascularization in the Matrigel injected area. Ch, choroids; M, Matrigel, R retina. Scale bar: 200 µm). ( C ) Quantitative analysis shows no difference in the levels of neovascularization between HMGB1-treated eyes compared to control eyes. ( D ) VEGF-A expression was not changed in glial cells (astrocytea and microglia) treated with HMGB-1 and PBS (control). ( E ) Examination by western blot of vitreous humor from both hyperoxia-injured and room air control animals (obtained from postnatal days 15 and 17 pups) did not show a statistically significant difference between them. Results of analysis of western blots (top) are expressed as a percentage of corresponding value in the control eyes ± SEM (n = 6).

    Article Snippet: Proteins were blotted onto a PVDF membrane (Invitrogen, Carlsbad, CA) and incubated with HMGB-1 primary antibody (1∶1000, Abcam, Cambridge, MA).

    Techniques: Labeling, Fluorescence, Microscopy, Injection, Expressing, Western Blot

    Proposed mechanism of action of SM83 in cancer ascites. SM83 stimulates the reversal of macrophages from M2 to M1 phenotype. TNF secreted by M1 macrophages triggers necrotic death of the cancer cells within the ascitic fluid; the dying cells release HMGB-1 that, together with TNF, recruits neutrophils

    Journal: Cell Death & Disease

    Article Title: Smac mimetics induce inflammation and necrotic tumour cell death by modulating macrophage activity

    doi: 10.1038/cddis.2013.449

    Figure Lengend Snippet: Proposed mechanism of action of SM83 in cancer ascites. SM83 stimulates the reversal of macrophages from M2 to M1 phenotype. TNF secreted by M1 macrophages triggers necrotic death of the cancer cells within the ascitic fluid; the dying cells release HMGB-1 that, together with TNF, recruits neutrophils

    Article Snippet: After saturation with non-fat dry milk-PBS, filters were hybridised with anti-HMGB-1 Ab (Abcam, 1:2000).

    Techniques:

    SM83 treatment promotes peritoneal neutrophil recruitment and activation. Cells were harvested from the ascitic fluid of mice treated with 5 mg/kg SM83. ( a ) Immunofluorescence for CD11b (green) and Gr-1 (red) was performed on Cytospin cell preparations. SM83 treatment induced a massive recruitment of neutrophils (CD11b + Gr-1 + ) at 24 h but not at earlier time points. ( b ) Dot blot of HMGB-1 (left panel) was performed on cleared ascitic fluids collected from untreated (un) or treated mice at 3, 6 and 24 h after a single injection of 5 mg/kg SM83. Right panel, loading control. ( c ) Infiltration of neutrophils (Gr-1; red) and HMGB-1 expression in dying tumour cells (green) in ascites untreated (upper row) and treated for 24 h (lower row) with a single injection of SM83. Left and right panels show two different magnifications ( × 10 and × 40). ( d ) PMN migration assessed by Transwell assay. Wild-type PMN from BALB/c mice (WT) or TNF-R1-deficient PMN from TNF-R1-KO mice (KO) were seeded into the upper chamber in the absence or presence of the HMGB-1 inhibitor glycyrrhizin (GLZ), whereas the ascitic fluid of mice untreated or treated for 6 h (1:20 in medium) was added to the lower chamber of the Transwell insert. PMN were left to migrate overnight, harvested and counted. ( e ) Activation of wild-type PMNs was colorimetrically evaluated on the basis of the ability of cells to oxidise the cytochrome c in presence of the ascitic fluid collected from mice 6 h after treating with a single injection of SM83. The experiment was also performed in the presence of GLZ and the TNF inhibitor etanercept. ( f ) Tumour cell counts in the ascites of untreated mice (UN), mice treated with a single injection of SM83 alone or mice treated with SM83 24 h after depletion of neutrophils by injection with the 1A8 mAb. ( g ) BALB/c mice were injected i.p. with Meth A cells and treated with 1A8 alone (▪) or in combination with 5 mg/kg SM83 (□), starting from day 7

    Journal: Cell Death & Disease

    Article Title: Smac mimetics induce inflammation and necrotic tumour cell death by modulating macrophage activity

    doi: 10.1038/cddis.2013.449

    Figure Lengend Snippet: SM83 treatment promotes peritoneal neutrophil recruitment and activation. Cells were harvested from the ascitic fluid of mice treated with 5 mg/kg SM83. ( a ) Immunofluorescence for CD11b (green) and Gr-1 (red) was performed on Cytospin cell preparations. SM83 treatment induced a massive recruitment of neutrophils (CD11b + Gr-1 + ) at 24 h but not at earlier time points. ( b ) Dot blot of HMGB-1 (left panel) was performed on cleared ascitic fluids collected from untreated (un) or treated mice at 3, 6 and 24 h after a single injection of 5 mg/kg SM83. Right panel, loading control. ( c ) Infiltration of neutrophils (Gr-1; red) and HMGB-1 expression in dying tumour cells (green) in ascites untreated (upper row) and treated for 24 h (lower row) with a single injection of SM83. Left and right panels show two different magnifications ( × 10 and × 40). ( d ) PMN migration assessed by Transwell assay. Wild-type PMN from BALB/c mice (WT) or TNF-R1-deficient PMN from TNF-R1-KO mice (KO) were seeded into the upper chamber in the absence or presence of the HMGB-1 inhibitor glycyrrhizin (GLZ), whereas the ascitic fluid of mice untreated or treated for 6 h (1:20 in medium) was added to the lower chamber of the Transwell insert. PMN were left to migrate overnight, harvested and counted. ( e ) Activation of wild-type PMNs was colorimetrically evaluated on the basis of the ability of cells to oxidise the cytochrome c in presence of the ascitic fluid collected from mice 6 h after treating with a single injection of SM83. The experiment was also performed in the presence of GLZ and the TNF inhibitor etanercept. ( f ) Tumour cell counts in the ascites of untreated mice (UN), mice treated with a single injection of SM83 alone or mice treated with SM83 24 h after depletion of neutrophils by injection with the 1A8 mAb. ( g ) BALB/c mice were injected i.p. with Meth A cells and treated with 1A8 alone (▪) or in combination with 5 mg/kg SM83 (□), starting from day 7

    Article Snippet: After saturation with non-fat dry milk-PBS, filters were hybridised with anti-HMGB-1 Ab (Abcam, 1:2000).

    Techniques: Activation Assay, Mouse Assay, Immunofluorescence, Dot Blot, Injection, Expressing, Migration, Transwell Assay

    RAGE binding of S100P, S100A4, and HMGB-1 was inhibited by an S100P-derived RAGE antagonistic peptide (RAP)

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    Article Title: S100P-DERIVED RAGE ANTAGONISTIC PEPTIDE (RAP) REDUCES TUMOR GROWTH AND METASTASIS

    doi: 10.1158/1078-0432.CCR-12-0221

    Figure Lengend Snippet: RAGE binding of S100P, S100A4, and HMGB-1 was inhibited by an S100P-derived RAGE antagonistic peptide (RAP)

    Article Snippet: RAGE and HMGB-1 were expressed in both normal and cancer cells.

    Techniques: Binding Assay, Derivative Assay

    Pancreatic cancer cells expressed and were stimulated by RAGE and its ligands S100P, S100A4, and HMGB-1

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    Article Title: S100P-DERIVED RAGE ANTAGONISTIC PEPTIDE (RAP) REDUCES TUMOR GROWTH AND METASTASIS

    doi: 10.1158/1078-0432.CCR-12-0221

    Figure Lengend Snippet: Pancreatic cancer cells expressed and were stimulated by RAGE and its ligands S100P, S100A4, and HMGB-1

    Article Snippet: RAGE and HMGB-1 were expressed in both normal and cancer cells.

    Techniques:

    HMGB-1–induced changes in the expression of SVEC surface adhesion molecules. (A) Representative immunofluorescent staining of β1-integrin in untreated and TNF-α, SDF-1α or HMGB-1–treated SVEC. (B) Number of SVEC showing β1-integrin polarization within the groups. (C) Representative images of P-selectin expression on SVEC plasmalemma in untreated and TNF-α, SDF-1α or HMGB-1–treated cells. (D) Number of SVEC showing P-selectin redistribution after stimulation with different cytokines. (E) Confocal images of ICAM-1 expression patterns on SVEC membrane. (F) Quantity of cells presenting ICAM-1 polarization after preconditioning with TNF-α, SDF-1α or HMGB-1 (* P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: HMGB-1 induces c-kit+ cell microvascular rolling and adhesion via both toll-like receptor-2 and toll-like receptor-4 of endothelial cells

    doi: 10.1111/j.1582-4934.2011.01381.x

    Figure Lengend Snippet: HMGB-1–induced changes in the expression of SVEC surface adhesion molecules. (A) Representative immunofluorescent staining of β1-integrin in untreated and TNF-α, SDF-1α or HMGB-1–treated SVEC. (B) Number of SVEC showing β1-integrin polarization within the groups. (C) Representative images of P-selectin expression on SVEC plasmalemma in untreated and TNF-α, SDF-1α or HMGB-1–treated cells. (D) Number of SVEC showing P-selectin redistribution after stimulation with different cytokines. (E) Confocal images of ICAM-1 expression patterns on SVEC membrane. (F) Quantity of cells presenting ICAM-1 polarization after preconditioning with TNF-α, SDF-1α or HMGB-1 (* P

    Article Snippet: It is reasonable to speculate HMGB-1 mediates c-kit+ cell recruitment via both the TLR-2 and TLR-4 signalling of endothelial cells.

    Techniques: Expressing, Staining

    The mRNA level of P-selectin in presence or absence of TLR-2 and TLR-4. Quantitative real-time PCR analysis in ‘Control’, ‘HMGB-1’, ‘TLR-2ko’ and ‘TLR-4ko’ groups. P-selectin mRNA is significantly up-regulated by HMGB-1 only when TLR-2 is functional. The average mRNA expression level of eNOS and c-kit in ‘Control’ cremasters was arbitrarily given a value of 1 (line) (** P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: HMGB-1 induces c-kit+ cell microvascular rolling and adhesion via both toll-like receptor-2 and toll-like receptor-4 of endothelial cells

    doi: 10.1111/j.1582-4934.2011.01381.x

    Figure Lengend Snippet: The mRNA level of P-selectin in presence or absence of TLR-2 and TLR-4. Quantitative real-time PCR analysis in ‘Control’, ‘HMGB-1’, ‘TLR-2ko’ and ‘TLR-4ko’ groups. P-selectin mRNA is significantly up-regulated by HMGB-1 only when TLR-2 is functional. The average mRNA expression level of eNOS and c-kit in ‘Control’ cremasters was arbitrarily given a value of 1 (line) (** P

    Article Snippet: It is reasonable to speculate HMGB-1 mediates c-kit+ cell recruitment via both the TLR-2 and TLR-4 signalling of endothelial cells.

    Techniques: Real-time Polymerase Chain Reaction, Functional Assay, Expressing

    HMGB-1–mediated c-kit + cell rolling and adhesion on cremaster muscle. (A) Percentage of rolling WT c-kit + cells in TLRs knockout mice. (B) Quantity of adherent WT c-kit + cells in TLRs knockout mice. (C) Percentage of rolling TLR-2 (−/−) and Tlr4 (LPS-del)c-kit + cells in WT animals. (D) Number of adherent TLR-2 (−/−) and Tlr4 (LPS-del) c-kit + cells in WT animals (* P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: HMGB-1 induces c-kit+ cell microvascular rolling and adhesion via both toll-like receptor-2 and toll-like receptor-4 of endothelial cells

    doi: 10.1111/j.1582-4934.2011.01381.x

    Figure Lengend Snippet: HMGB-1–mediated c-kit + cell rolling and adhesion on cremaster muscle. (A) Percentage of rolling WT c-kit + cells in TLRs knockout mice. (B) Quantity of adherent WT c-kit + cells in TLRs knockout mice. (C) Percentage of rolling TLR-2 (−/−) and Tlr4 (LPS-del)c-kit + cells in WT animals. (D) Number of adherent TLR-2 (−/−) and Tlr4 (LPS-del) c-kit + cells in WT animals (* P

    Article Snippet: It is reasonable to speculate HMGB-1 mediates c-kit+ cell recruitment via both the TLR-2 and TLR-4 signalling of endothelial cells.

    Techniques: Knock-Out, Mouse Assay

    HMGB-1 increases eNOS and c-kit expression in presence of TLR-2. Quantitative real-time PCR and confocal microscopy analysis of stem cell homing signals in cremaster muscle. (A) eNOS and c-kit genes expression in ‘Control’, ‘HMGB-1’, ‘TLR-2ko’ and ‘TLR-4ko’ groups. The average mRNA expression level of eNOS and c-kit in ‘Control’ cremaster muscle tissue was arbitrarily given a value of 1 (line) (* P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: HMGB-1 induces c-kit+ cell microvascular rolling and adhesion via both toll-like receptor-2 and toll-like receptor-4 of endothelial cells

    doi: 10.1111/j.1582-4934.2011.01381.x

    Figure Lengend Snippet: HMGB-1 increases eNOS and c-kit expression in presence of TLR-2. Quantitative real-time PCR and confocal microscopy analysis of stem cell homing signals in cremaster muscle. (A) eNOS and c-kit genes expression in ‘Control’, ‘HMGB-1’, ‘TLR-2ko’ and ‘TLR-4ko’ groups. The average mRNA expression level of eNOS and c-kit in ‘Control’ cremaster muscle tissue was arbitrarily given a value of 1 (line) (* P

    Article Snippet: It is reasonable to speculate HMGB-1 mediates c-kit+ cell recruitment via both the TLR-2 and TLR-4 signalling of endothelial cells.

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Confocal Microscopy

    Endogenous leukocyte adhesion on cremaster muscle 15 min. after direct HMGB-1 superfusion. (A) Number (n/mm 2 ) of adherent leukocytes in ‘Control’ and ‘HMGB-1’ groups. (B) Quantitative real-time PCR analysis of the pro-inflammatory signals β1-integrin and CD45 of ‘Control’, ‘HMGB-1’, ‘TLR-2ko’ and ‘TLR-4ko’ groups. The average mRNA expression level of β1-intergrin and CD45 and c-kit in ‘Control’ cremasters was arbitrarily given a value of 1 (line) (* P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: HMGB-1 induces c-kit+ cell microvascular rolling and adhesion via both toll-like receptor-2 and toll-like receptor-4 of endothelial cells

    doi: 10.1111/j.1582-4934.2011.01381.x

    Figure Lengend Snippet: Endogenous leukocyte adhesion on cremaster muscle 15 min. after direct HMGB-1 superfusion. (A) Number (n/mm 2 ) of adherent leukocytes in ‘Control’ and ‘HMGB-1’ groups. (B) Quantitative real-time PCR analysis of the pro-inflammatory signals β1-integrin and CD45 of ‘Control’, ‘HMGB-1’, ‘TLR-2ko’ and ‘TLR-4ko’ groups. The average mRNA expression level of β1-intergrin and CD45 and c-kit in ‘Control’ cremasters was arbitrarily given a value of 1 (line) (* P

    Article Snippet: It is reasonable to speculate HMGB-1 mediates c-kit+ cell recruitment via both the TLR-2 and TLR-4 signalling of endothelial cells.

    Techniques: Real-time Polymerase Chain Reaction, Expressing

    Effects of direct HMGB-1 superfusion of cremaster muscle on c-kit + cell rolling and adhesion 15 min. after treatment. (A) Representative intravital fluorescence microscopy images of rolling and adherent c-kit + cells. (B) Percentage of rolling c-kit + cells in ‘Control’, ‘HMGB-1’, ‘LPS’ and ‘MALP-2’ groups. (C) Amount of adherent c-kit + cells in ‘Control’, ‘HMGB-1’, ‘LPS’ and ‘MALP-2’ groups (* P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: HMGB-1 induces c-kit+ cell microvascular rolling and adhesion via both toll-like receptor-2 and toll-like receptor-4 of endothelial cells

    doi: 10.1111/j.1582-4934.2011.01381.x

    Figure Lengend Snippet: Effects of direct HMGB-1 superfusion of cremaster muscle on c-kit + cell rolling and adhesion 15 min. after treatment. (A) Representative intravital fluorescence microscopy images of rolling and adherent c-kit + cells. (B) Percentage of rolling c-kit + cells in ‘Control’, ‘HMGB-1’, ‘LPS’ and ‘MALP-2’ groups. (C) Amount of adherent c-kit + cells in ‘Control’, ‘HMGB-1’, ‘LPS’ and ‘MALP-2’ groups (* P

    Article Snippet: It is reasonable to speculate HMGB-1 mediates c-kit+ cell recruitment via both the TLR-2 and TLR-4 signalling of endothelial cells.

    Techniques: Fluorescence, Microscopy

    Effects of extracorporeal blood purification (EBP) on high-mobility group box 1 (HMGB-1) Plasma HMGB-1 levels are shown over time (mean ± s.e.m., ng/ml). * P

    Journal: Kidney International

    Article Title: Acute removal of common sepsis mediators does not explain the effects of extracorporeal blood purification in experimental sepsis

    doi: 10.1038/ki.2011.320

    Figure Lengend Snippet: Effects of extracorporeal blood purification (EBP) on high-mobility group box 1 (HMGB-1) Plasma HMGB-1 levels are shown over time (mean ± s.e.m., ng/ml). * P

    Article Snippet: HMGB-1 was measured using an enzyme-linked immunosorbent assay (Shino-Test Corporation, Chiba, Japan, measurement range 0–80 ng/ml).

    Techniques: Purification

    Reduced expression of proinflammatory factors in mesenchymal stem cells (MSCs) overexpressing the soluble receptor for advanced glycation end products(sRAGE). ( A ) Schematic representation of sRAGE DNA vector constructs. ( B ) MSCs were transfected with mock or sRAGE vector using the X-tremeGENE HP reagent for 3 days. RAGE and high-mobility group box-1 (HMGB-1) levels in MSCs and sRAGE-MSCs were measured by ELISA and western blotting. ( C ) Transcript levels of vascular endothelial growth factor ( VEGF ), interleukin-1β ( IL-1β ), IL-6 , HMGB-1 , IL-10 , transforming growth factor-β ( TGF-β ), indoleamine 2,3-dioxygenase ( IDO ), and hepatocyte growth factor ( HGF ) were determined using real-time PCR. Data represent the mean ± s.d. (bar) values from three independent experiments. * P

    Journal: Scientific Reports

    Article Title: Overexpression of soluble RAGE in mesenchymal stem cells enhances their immunoregulatory potential for cellular therapy in autoimmune arthritis

    doi: 10.1038/srep35933

    Figure Lengend Snippet: Reduced expression of proinflammatory factors in mesenchymal stem cells (MSCs) overexpressing the soluble receptor for advanced glycation end products(sRAGE). ( A ) Schematic representation of sRAGE DNA vector constructs. ( B ) MSCs were transfected with mock or sRAGE vector using the X-tremeGENE HP reagent for 3 days. RAGE and high-mobility group box-1 (HMGB-1) levels in MSCs and sRAGE-MSCs were measured by ELISA and western blotting. ( C ) Transcript levels of vascular endothelial growth factor ( VEGF ), interleukin-1β ( IL-1β ), IL-6 , HMGB-1 , IL-10 , transforming growth factor-β ( TGF-β ), indoleamine 2,3-dioxygenase ( IDO ), and hepatocyte growth factor ( HGF ) were determined using real-time PCR. Data represent the mean ± s.d. (bar) values from three independent experiments. * P

    Article Snippet: Measurement of cytokine and IgG levels The concentrations of VEGF, IL-1β, IL-6, RAGE, and HMGB-1 (ABNOVA Corp., Taiwan) in culture supernatants and serum samples were measured using a sandwich enzyme-linked immunosorbent assay (ELISA) (DuoSet; R & D Systems).

    Techniques: Expressing, Plasmid Preparation, Construct, Transfection, Enzyme-linked Immunosorbent Assay, Western Blot, Real-time Polymerase Chain Reaction

    LPS-stimulated increase in the expression of proinflammatory factors in mesenchymal stem cells (MSCs). MSCs (2.5 × 10 5 ) remained non-stimulated or were stimulated with lipopolysaccharide (LPS; 1 μg/mL) for 2 days. ( A ) mRNA expression of vascular endothelial growth factor ( VEGF ), interleukin-1β ( IL-1β ), IL-6 , and high-mobility group box-1 ( HMGB-1 ) was determined using real-time PCR. Data represent the mean ± s.d. (bars) values of three independent experiments. ( B ) VEGF, IL-1β, IL-6, and HMGB-1 concentrations in culture supernatants were measured using ELISA. ( C ) SDS-PAGE of protein lysates was followed by western blot analysis for HMGB-1, receptor for advanced glycation end products (RAGE), and β-actin. * P

    Journal: Scientific Reports

    Article Title: Overexpression of soluble RAGE in mesenchymal stem cells enhances their immunoregulatory potential for cellular therapy in autoimmune arthritis

    doi: 10.1038/srep35933

    Figure Lengend Snippet: LPS-stimulated increase in the expression of proinflammatory factors in mesenchymal stem cells (MSCs). MSCs (2.5 × 10 5 ) remained non-stimulated or were stimulated with lipopolysaccharide (LPS; 1 μg/mL) for 2 days. ( A ) mRNA expression of vascular endothelial growth factor ( VEGF ), interleukin-1β ( IL-1β ), IL-6 , and high-mobility group box-1 ( HMGB-1 ) was determined using real-time PCR. Data represent the mean ± s.d. (bars) values of three independent experiments. ( B ) VEGF, IL-1β, IL-6, and HMGB-1 concentrations in culture supernatants were measured using ELISA. ( C ) SDS-PAGE of protein lysates was followed by western blot analysis for HMGB-1, receptor for advanced glycation end products (RAGE), and β-actin. * P

    Article Snippet: Measurement of cytokine and IgG levels The concentrations of VEGF, IL-1β, IL-6, RAGE, and HMGB-1 (ABNOVA Corp., Taiwan) in culture supernatants and serum samples were measured using a sandwich enzyme-linked immunosorbent assay (ELISA) (DuoSet; R & D Systems).

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, SDS Page, Western Blot

    In vitro characterization of the different cell death modalities induced in CT26 cells. (A) FACS analysis of cells treated in vitro with the indicated agents as specified in Materials and methods. ZVAD, Z-VAD-fmk. Numbers indicate the percentage of cells (X ± SD, n = 5) in each quadrant. (B) Immunoblot analyses of cells treated as in A. Cellular extracts were subjected to the immunodetection of activated caspase 3 (Casp3a), HMGB-1, and HSP-70. (C) TUNEL staining (green) of cells counterstained with DAPI (blue). The percentage of TUNEL + cells (X ± SEM, n = 3) was determined. (D) Transmission electron microscopy. Representative microphotographs are shown. Apoptotic cells showing chromatin condensation are labeled with an “A.” (E) Cells treated with the indicated agents as in A were washed and plated to determine the frequency of surviving clones, defining the control value of untreated cells as 100%. Results are representative of three independent experiments.

    Journal: The Journal of Experimental Medicine

    Article Title: Caspase-dependent immunogenicity of doxorubicin-induced tumor cell death

    doi: 10.1084/jem.20050915

    Figure Lengend Snippet: In vitro characterization of the different cell death modalities induced in CT26 cells. (A) FACS analysis of cells treated in vitro with the indicated agents as specified in Materials and methods. ZVAD, Z-VAD-fmk. Numbers indicate the percentage of cells (X ± SD, n = 5) in each quadrant. (B) Immunoblot analyses of cells treated as in A. Cellular extracts were subjected to the immunodetection of activated caspase 3 (Casp3a), HMGB-1, and HSP-70. (C) TUNEL staining (green) of cells counterstained with DAPI (blue). The percentage of TUNEL + cells (X ± SEM, n = 3) was determined. (D) Transmission electron microscopy. Representative microphotographs are shown. Apoptotic cells showing chromatin condensation are labeled with an “A.” (E) Cells treated with the indicated agents as in A were washed and plated to determine the frequency of surviving clones, defining the control value of untreated cells as 100%. Results are representative of three independent experiments.

    Article Snippet: Primary antibodies detecting activated caspase 3 (dilution 1/1,000; Cell Signaling Technology), HSP70 (dilution 1/1,000; Stratagene) or 2 μg/ml HMGB-1 (BD Biosciences) were revealed with the appropriate horseradish peroxidase–labeled secondary antibody (Southern Biotechnology Associates, Inc.) and detected by enhanced chemiluminescence (Pierce Chemical Co.).

    Techniques: In Vitro, FACS, Immunodetection, TUNEL Assay, Staining, Transmission Assay, Electron Microscopy, Labeling, Clone Assay

    ( A ) Rate of early allograft dysfunction (EAD) with effluent above HMGB-1 and below 580 ng/ml. With HMGB-1 values above 580 ng/ml, only 1 out of 13 patients did not develop EAD. ( B ) Rate of initial non-function (INF) with effluent HMGB-1 above and below 1608 ng/ml. With HMGB-1 values below 1608 ng/ml, only 1 out of 26 patients developed INF.

    Journal: Annals of Transplantation

    Article Title: Evaluation of Graft Effluent High Mobility Group Box-1 (HMGB-1) for Prediction of Outcome After Liver Transplantation

    doi: 10.12659/AOT.909165

    Figure Lengend Snippet: ( A ) Rate of early allograft dysfunction (EAD) with effluent above HMGB-1 and below 580 ng/ml. With HMGB-1 values above 580 ng/ml, only 1 out of 13 patients did not develop EAD. ( B ) Rate of initial non-function (INF) with effluent HMGB-1 above and below 1608 ng/ml. With HMGB-1 values below 1608 ng/ml, only 1 out of 26 patients developed INF.

    Article Snippet: Measurement of high mobility group box-1 (HMGB-1) A commercially available, enzyme-linked immunosorbent assay (ELISA), designed for serum measurements of HMGB-1 (IBL International, Germany), was applied for the analysis of HMGB-1 concentrations in the effluent.

    Techniques:

    ( A ) Effluent HMGB-1 values as a function of early allograft dysfunction (EAD). Dots represent individual recipients and horizontal bars indicate the mean (n=30; p=.031). ( B ) Effluent HMGB-1 values as a function of initial graft non-function (INF). Dots represent individual recipients; horizontal bars indicate the mean (n=30; p=.139).

    Journal: Annals of Transplantation

    Article Title: Evaluation of Graft Effluent High Mobility Group Box-1 (HMGB-1) for Prediction of Outcome After Liver Transplantation

    doi: 10.12659/AOT.909165

    Figure Lengend Snippet: ( A ) Effluent HMGB-1 values as a function of early allograft dysfunction (EAD). Dots represent individual recipients and horizontal bars indicate the mean (n=30; p=.031). ( B ) Effluent HMGB-1 values as a function of initial graft non-function (INF). Dots represent individual recipients; horizontal bars indicate the mean (n=30; p=.139).

    Article Snippet: Measurement of high mobility group box-1 (HMGB-1) A commercially available, enzyme-linked immunosorbent assay (ELISA), designed for serum measurements of HMGB-1 (IBL International, Germany), was applied for the analysis of HMGB-1 concentrations in the effluent.

    Techniques:

    Plasma CTRP-3 (a) and HMGB-1 (b) concentrations in different subgroups and in males and females ((c) and (d)). Data were presented as means ± standard deviation. Differences between multiple groups were tested by analysis of variance (ANOVA) for continuous variables. P for trend was estimated by a linear-by-linear association of the chi-square test. ∗ P

    Journal: Journal of Diabetes Research

    Article Title: Plasma C1q/TNF-Related Protein-3 (CTRP-3) and High-Mobility Group Box-1 (HMGB-1) Concentrations in Subjects with Prediabetes and Type 2 Diabetes

    doi: 10.1155/2016/9438760

    Figure Lengend Snippet: Plasma CTRP-3 (a) and HMGB-1 (b) concentrations in different subgroups and in males and females ((c) and (d)). Data were presented as means ± standard deviation. Differences between multiple groups were tested by analysis of variance (ANOVA) for continuous variables. P for trend was estimated by a linear-by-linear association of the chi-square test. ∗ P

    Article Snippet: Assessment of Plasma CTRP-3, HMGB-1, and IL-6 Levels Plasma CTRP-3, HMGB-1, and IL-6 levels were determined by commercial ELISA kits according to the manufacturers' instructions (Human ELISA kit, Uscn Life Science Inc., Wuhan, China).

    Techniques: Standard Deviation

    Elimination of RAGE does not influence remote organ (liver) injury and systemic inflammation following intestinal IR . Mice were subjected to 30 min mesenteric artery occlusion, followed by 150 min reperfusion. Peripheral blood samples were collected from WT-SHAM, WT-IR, and RAGE −/− IR groups for enzyme activity and pro-inflammatory markers. (A,B) Activities of liver enzymes ALT (A) and ALP (B) measured as markers of liver injury. (C,D) Levels of pro-inflammatory mediators HMGB-1 (C) and IL-6 (D) . Data are presented as mean ± SEM, n = 5 (WT-SHAM); n = 13 (WT-IR); n = 15 (RAGE −/− IR) where * p

    Journal: Frontiers in Immunology

    Article Title: The Receptor for Advanced Glycation Endproducts Does Not Contribute to Pathology in a Mouse Mesenteric Ischemia/Reperfusion-Induced Injury Model

    doi: 10.3389/fimmu.2015.00614

    Figure Lengend Snippet: Elimination of RAGE does not influence remote organ (liver) injury and systemic inflammation following intestinal IR . Mice were subjected to 30 min mesenteric artery occlusion, followed by 150 min reperfusion. Peripheral blood samples were collected from WT-SHAM, WT-IR, and RAGE −/− IR groups for enzyme activity and pro-inflammatory markers. (A,B) Activities of liver enzymes ALT (A) and ALP (B) measured as markers of liver injury. (C,D) Levels of pro-inflammatory mediators HMGB-1 (C) and IL-6 (D) . Data are presented as mean ± SEM, n = 5 (WT-SHAM); n = 13 (WT-IR); n = 15 (RAGE −/− IR) where * p

    Article Snippet: Inflammatory Protein Levels Plasma cytokines, HMGB-1, and IL-6 and complement factor C3a levels were measured by enzyme-linked immunosorbent (ELISA) kits (Chondrex, USA; BD Biosciences, Australia), according to their manufacturers’ instructions.

    Techniques: Mouse Assay, Activity Assay, ALP Assay

    SP-A interaction with Mp-stimulated DCs Bone marrow derived dendritic cells were cultured for 6 days in the presence of GM-CSF, purified and stimulated with Mp (10 cfu/cell) for 16 hours in the presence or absence of SP-A (50 μg/ml). Supernatants and lysates were harvested for analysis by SDS-PAGE and western immunoblotting for either HMGB-1, SP A or GAPDH. A , immature dendritic cells were used immediately after purification on day 6 or B , mature dendritic cells were stimulated for 24 hours in the presence of LPS prior to studies with Mp. C , dendritic cells were either treated for 16 hours with nothing (lane 1), pre-incubated with SP-A, washed, then stimulated with media (lane 2) or Mp (lane 3), or stimulated with SP-A coated Mp (lane 4) or non-coated Mp (lane 5). D , dendritic cells were pre-incubated with a TLR-2 neutralizing antibody or isotype control antibody prior to stimulation with Mp for 16 hours. Blots are representative from experiments conducted from 3 independent BMDC cultures.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Surfactant Protein-A Inhibits Mycoplasma-Induced Dendritic Cell Maturation through Regulation of HMGB-1 Cytokine Activity

    doi: 10.4049/jimmunol.1000387

    Figure Lengend Snippet: SP-A interaction with Mp-stimulated DCs Bone marrow derived dendritic cells were cultured for 6 days in the presence of GM-CSF, purified and stimulated with Mp (10 cfu/cell) for 16 hours in the presence or absence of SP-A (50 μg/ml). Supernatants and lysates were harvested for analysis by SDS-PAGE and western immunoblotting for either HMGB-1, SP A or GAPDH. A , immature dendritic cells were used immediately after purification on day 6 or B , mature dendritic cells were stimulated for 24 hours in the presence of LPS prior to studies with Mp. C , dendritic cells were either treated for 16 hours with nothing (lane 1), pre-incubated with SP-A, washed, then stimulated with media (lane 2) or Mp (lane 3), or stimulated with SP-A coated Mp (lane 4) or non-coated Mp (lane 5). D , dendritic cells were pre-incubated with a TLR-2 neutralizing antibody or isotype control antibody prior to stimulation with Mp for 16 hours. Blots are representative from experiments conducted from 3 independent BMDC cultures.

    Article Snippet: Gels were transferred onto Nitrocellulose membrane and blocked with 5% block (milk in TBS) and labeled with an HMGB-1 antibody (Abcam, ab12029 or ab65003) overnight at 1:1500.

    Techniques: Derivative Assay, Cell Culture, Purification, SDS Page, Western Blot, Incubation

    SP-A inhibition of HMGB-1 secretion from human cells A , THP-1 cells or B , NHBE cells were incubated with 50 μg/ml purified human SP-A (+) or an equivalent volume of sterile Tris buffer (−) for 2 hours prior to stimulation with 10 Mp cfu/cell or with saline only (0). Cell free supernatants and lysates were harvested 16 hours post stimulation and HMGB-1 and GAPDH expression were assessed by Western analysis. Picture is representative of 2 experiments.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Surfactant Protein-A Inhibits Mycoplasma-Induced Dendritic Cell Maturation through Regulation of HMGB-1 Cytokine Activity

    doi: 10.4049/jimmunol.1000387

    Figure Lengend Snippet: SP-A inhibition of HMGB-1 secretion from human cells A , THP-1 cells or B , NHBE cells were incubated with 50 μg/ml purified human SP-A (+) or an equivalent volume of sterile Tris buffer (−) for 2 hours prior to stimulation with 10 Mp cfu/cell or with saline only (0). Cell free supernatants and lysates were harvested 16 hours post stimulation and HMGB-1 and GAPDH expression were assessed by Western analysis. Picture is representative of 2 experiments.

    Article Snippet: Gels were transferred onto Nitrocellulose membrane and blocked with 5% block (milk in TBS) and labeled with an HMGB-1 antibody (Abcam, ab12029 or ab65003) overnight at 1:1500.

    Techniques: Inhibition, Incubation, Purification, Expressing, Western Blot

    Inhibition of HMGB-1 cytokine activity limits DC maturation to Mp A , Western analysis of cell free BAL harvested 3 days after Mp infection of WT and SP-A −/− mice for HMGB-1 expression and compared to HMGB-1 levels measured in saline treated mice. The same total volume was loaded for each sample. Control (C) is brain lysate. Representative of 3 separate experiments. B , WT and SP-A −/− mice were treated with Glycyrrhizin (10 mg/kg body weight) or vehicle (saline) prior to and during infection with Mp. Three days after infection, MLNs were harvested, cells collected after enzymatic digestion and density gradient centrifugation to enrich for DCs, and labeled with fluorescent antibodies for flow cytometry analysis. The number of MHCII hi CD11c + DCs from the MLNs that were CD86+ are shown. WT and SP-A −/− uninfected (U) mice were included as baseline controls. *p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Surfactant Protein-A Inhibits Mycoplasma-Induced Dendritic Cell Maturation through Regulation of HMGB-1 Cytokine Activity

    doi: 10.4049/jimmunol.1000387

    Figure Lengend Snippet: Inhibition of HMGB-1 cytokine activity limits DC maturation to Mp A , Western analysis of cell free BAL harvested 3 days after Mp infection of WT and SP-A −/− mice for HMGB-1 expression and compared to HMGB-1 levels measured in saline treated mice. The same total volume was loaded for each sample. Control (C) is brain lysate. Representative of 3 separate experiments. B , WT and SP-A −/− mice were treated with Glycyrrhizin (10 mg/kg body weight) or vehicle (saline) prior to and during infection with Mp. Three days after infection, MLNs were harvested, cells collected after enzymatic digestion and density gradient centrifugation to enrich for DCs, and labeled with fluorescent antibodies for flow cytometry analysis. The number of MHCII hi CD11c + DCs from the MLNs that were CD86+ are shown. WT and SP-A −/− uninfected (U) mice were included as baseline controls. *p

    Article Snippet: Gels were transferred onto Nitrocellulose membrane and blocked with 5% block (milk in TBS) and labeled with an HMGB-1 antibody (Abcam, ab12029 or ab65003) overnight at 1:1500.

    Techniques: Inhibition, Activity Assay, Western Blot, Infection, Mouse Assay, Expressing, Gradient Centrifugation, Labeling, Flow Cytometry, Cytometry

    The damage-associated molecules, HMGB-1 and ATP induce expression of IL-33 mRNA in sinonasal epithelial cells derived from recalcitrant CRSwNP subjects. Data is expressed as fold increase over unstimulated condition within individual subjects. * p= 0.046; **p=0.033

    Journal: International forum of allergy & rhinology

    Article Title: Damage-associated molecular patterns stimulate IL-33 expression in nasal polyp epithelial cells

    doi: 10.1002/alr.21237

    Figure Lengend Snippet: The damage-associated molecules, HMGB-1 and ATP induce expression of IL-33 mRNA in sinonasal epithelial cells derived from recalcitrant CRSwNP subjects. Data is expressed as fold increase over unstimulated condition within individual subjects. * p= 0.046; **p=0.033

    Article Snippet: For HMGB-1 challenge, epithelial cells at the ALI were exposed to 100 ng/ml HMGB-1 (Sigma, St Louis, MO) in 250 microliters of media applied to the apical surface for 48 hours.

    Techniques: Expressing, Derivative Assay

    Stimulation of sinonasal epithelial cell expression of IL-33 with HMGB-1 and ATP. Sinonasal epithelial cells grown at the air-liquid interface were exposed to the damage-associated molecules, HMGB-1 (100 ng/ml) for 24 hours, or ATP (100 μM) for 8 hours. A marked increase in nuclear expression of IL-33 protein was observed in recalcitrant CRSwNP subjects, although the mean increase in nuclear immunofluoresence did not achieve statistical significance for the group as a whole. (A/B: pre- and post-HMGB-1 exposure; C/D: pre- and post-ATP exposure). E: Graphical representation of increase in mean IL-33 immunostaining following exposure to HMGB-1 and ATP, across all subjects (p=ns).

    Journal: International forum of allergy & rhinology

    Article Title: Damage-associated molecular patterns stimulate IL-33 expression in nasal polyp epithelial cells

    doi: 10.1002/alr.21237

    Figure Lengend Snippet: Stimulation of sinonasal epithelial cell expression of IL-33 with HMGB-1 and ATP. Sinonasal epithelial cells grown at the air-liquid interface were exposed to the damage-associated molecules, HMGB-1 (100 ng/ml) for 24 hours, or ATP (100 μM) for 8 hours. A marked increase in nuclear expression of IL-33 protein was observed in recalcitrant CRSwNP subjects, although the mean increase in nuclear immunofluoresence did not achieve statistical significance for the group as a whole. (A/B: pre- and post-HMGB-1 exposure; C/D: pre- and post-ATP exposure). E: Graphical representation of increase in mean IL-33 immunostaining following exposure to HMGB-1 and ATP, across all subjects (p=ns).

    Article Snippet: For HMGB-1 challenge, epithelial cells at the ALI were exposed to 100 ng/ml HMGB-1 (Sigma, St Louis, MO) in 250 microliters of media applied to the apical surface for 48 hours.

    Techniques: Expressing, Immunostaining

    TAK-242 inhibits both LPS-induced and HMGB-1-induced TNF-α production in RAW264.7 cells. Cells were cultured with 0.5 ng·mL −1 LPS or 10 µg·mL −1 HMGB-1 for 20 h in the presence of 0.1 ng·mL −1

    Journal: British Journal of Pharmacology

    Article Title: Analysis of binding site for the novel small-molecule TLR4 signal transduction inhibitor TAK-242 and its therapeutic effect on mouse sepsis model

    doi: 10.1111/j.1476-5381.2009.00297.x

    Figure Lengend Snippet: TAK-242 inhibits both LPS-induced and HMGB-1-induced TNF-α production in RAW264.7 cells. Cells were cultured with 0.5 ng·mL −1 LPS or 10 µg·mL −1 HMGB-1 for 20 h in the presence of 0.1 ng·mL −1

    Article Snippet: HMGB-1 were purchased from R & D Systems (Minneapolis, MN, USA).

    Techniques: Cell Culture

    SiRNA HMGB-1 effect on TLR4 and NF-κB mRNA expression in RGC-5. ( A ) SiRNA HMGB-1 effect on TLR4 mRNA expression in RGC-5; ( B ) SiRNA HMGB-1 effect on NF-κB mRNA expression in RGC-5.* TLR-4 P=0.009; NF-κB P=0.017, compared with control; # TLR-4 P=0.033; NF-κB P=0.024, compared with high glucose group.

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: HMGB-1 as a Potential Target for the Treatment of Diabetic Retinopathy

    doi: 10.12659/MSM.894453

    Figure Lengend Snippet: SiRNA HMGB-1 effect on TLR4 and NF-κB mRNA expression in RGC-5. ( A ) SiRNA HMGB-1 effect on TLR4 mRNA expression in RGC-5; ( B ) SiRNA HMGB-1 effect on NF-κB mRNA expression in RGC-5.* TLR-4 P=0.009; NF-κB P=0.017, compared with control; # TLR-4 P=0.033; NF-κB P=0.024, compared with high glucose group.

    Article Snippet: SiRNA HMGB-1 transfection SiRNA HMGB-1 (Shanghai Genepharma, China) were transfected into RGC-5 cells using Lipofectamine 2000 reagent according to the manufacturer’s instructions.

    Techniques: Expressing

    SiRNA HMGB-1 effect on TLR4 and NF-κB protein expression in RGC-5.* TLR-4 P =0.041; NF-κB P =0.024, compared with control; # TLR-4 P =0.032; NF-κB P =0.027, compared with high glucose group.

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: HMGB-1 as a Potential Target for the Treatment of Diabetic Retinopathy

    doi: 10.12659/MSM.894453

    Figure Lengend Snippet: SiRNA HMGB-1 effect on TLR4 and NF-κB protein expression in RGC-5.* TLR-4 P =0.041; NF-κB P =0.024, compared with control; # TLR-4 P =0.032; NF-κB P =0.027, compared with high glucose group.

    Article Snippet: SiRNA HMGB-1 transfection SiRNA HMGB-1 (Shanghai Genepharma, China) were transfected into RGC-5 cells using Lipofectamine 2000 reagent according to the manufacturer’s instructions.

    Techniques: Expressing

    SiRNA HMGB-1 impact on RGC-5 cell survival. * P =0.026, compared with control; # P =0.037, compared with high glucose group.

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: HMGB-1 as a Potential Target for the Treatment of Diabetic Retinopathy

    doi: 10.12659/MSM.894453

    Figure Lengend Snippet: SiRNA HMGB-1 impact on RGC-5 cell survival. * P =0.026, compared with control; # P =0.037, compared with high glucose group.

    Article Snippet: SiRNA HMGB-1 transfection SiRNA HMGB-1 (Shanghai Genepharma, China) were transfected into RGC-5 cells using Lipofectamine 2000 reagent according to the manufacturer’s instructions.

    Techniques: