icam-1 Search Results


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  • 94
    Thermo Fisher icam 1
    Effects of SsnB on the LPS-induced <t>ICAM-1</t> and VCAM-1 expression in HUVECs. Cells were treated with SsnB and LPS as indicated for 24 h, were then lysed, and the protein levels were detected by Western blot analysis ( upper ). The blots were quantified by
    Icam 1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 1895 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore icam 1
    Effect of APC on the HMGB1-mediated expression of cell adhesion molecules in HUVECs. Confluent HUVECs were incubated with HMGB1 (1 μg/mL for 16 hours) after treating cells with indicated concentrations of APC for 3 hours. The cell surface expression of VCAM-1 (A), <t>ICAM-1</t> (B), and E-selectin (C) on HUVECs was measured by a cell-based ELISA as described in “Methods.” All results are shown as means ± SDs of 5 different experiments. * P
    Icam 1, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 361 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology icam 1
    Effect of DYSGT on ET-1, <t>ICAM-1,</t> and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P
    Icam 1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 2370 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Abcam icam 1
    RAS inhibitor attenuated the H 2 O 2 -induced increases in expressions of p53, <t>ICAM-1,</t> p-eNOS, p-AKT and p-mTOR via AKT/mTOR pathway. A – HCAECs were pre-treated with captopril or combined with AKT inhibitor or activator, then exposed to H 2 O 2 for 48 h. Cell lysate was analyzed for p53, ICAM-1, p-eNOS, p-Akt and p-mTOR protein levels by immunoblotting. B – Shows a column bar graph analysis *p
    Icam 1, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 1553 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Cell Signaling Technology Inc icam 1
    <t>ICAM-1</t> and CD11c co-localize during exosome-macrophage interactions. (A) Immunoblotting analysis reveals exosomes from the pancreatic cancer cell lines AsPC-1 and BxPC-3 are enriched in the surface-exposed proteins ICAM-1 and EpCAM, while CD9 is more broadly expressed. The pan-exosomal marker flotillin-1 is used as a loading control. (B) Co-localization of exosome proteins and macrophage proteins is demonstrated by immunostaining for the exosome marker ICAM-1 (green, panel 1) or the macrophage marker CD11c (red, panel 2) after mixing AsPC-1 exosomes with THP-1-derived, non-polarized macrophages. Panel 3 is a merged image showing co-localization of ICAM-1 and CD11c staining (yellow, indicated by an arrow), and is suggestive of ICAM-1 and CD11c protein-protein interaction. THP-1-derived macrophages not mixed with exosomes (cells only) show little ICAM-1 staining (green, panel 4), suggesting exosomes were the main source of the ICAM-1 signal. In the absence of exosomes, more CD11c is associated with the THP-1 cell surface (red, panel 5), and merged images of THP-1 only staining show few areas of signal co-localization (panel 6, yellow). Scale bar = 3.0 μm (C) Quantitation of ICAM-1:CD11c co-localized signal in THP-1 cells mixed with AsPC-1 exosomes or in THP-1 cells alone. *** p
    Icam 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 509 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Becton Dickinson icam 1
    CMH suppresses endothelial VCAM-1 and <t>ICAM-1</t> expression during EAE. a and c . Frozen sections of lumbar spinal cord taken from disease-free, EAE-normoxia or EAE-CMH mice at the peak symptomatic phase of EAE were stained for CD31 (AlexaFluor-488) and VCAM-1 (Cy-3) in panel A or CD31 (Cy-3) and ICAM-1 (AlexaFluor-488) in panel C. Scale bar = 100 μm (inset, scale bar = 50 μm). b and d . Quantification of VCAM-1 ( b ) and ICAM-1 expression ( d ). Results are expressed as the mean ± SEM ( n = 6 mice/group). Note that CMH markedly suppressed vascular expression of VCAM-1 and ICAM-1. ** p
    Icam 1, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 92/100, based on 901 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Santa Cruz Biotechnology antibodies icam 1
    Analysis of the miR-124 promoter and transcription factor Sp1 binds to miR-124 promoter (A) RAW264.7 cells were co-transfected with pRL-TK and a miR-124 promoter reporter plasmid containing various lengths of the miR-124 promoter. The first nucleotide of mature pre-miR-124 is assigned +1. Right panel shows the relative luciferase activities of these plasmids. Luciferase activity of the mock transfected empty vector pGL3-Basic was used for normalization. The data in graph were shown in mean ± SEM of 3 different transfections. (B) Schematic diagram of miR-124 genomic location in mouse chromosome 2. The promoter region from pre-197 to pre-27 was used for analysis of potential transcription factor binding sites. Two Sp1 binding sites are indicated as diamonds. The sequences of mutated sites are shown under the locus diagram. (C) Schematic representation of deletion mutants 1 and 2 in the full-length miR-124 promoter. (D) RAW264.7 cells were co-transfected with the above promoter reporter constructs and pRL-TK. Post-transfection for 36h, samples were collected and analyzed for dual luciferase activity. (E) Real-time qPCR and Western blot analysis of the expression of Sp1 after transfection with <t>ICAM-1</t> siRNA and negative control. ( * p
    Antibodies Icam 1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 25 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Thermo Fisher gene exp icam1 hs00164932 m1
    Amplification of poly (I:C)-mediated induction of cytokines, chemokines and adhesion molecules by TNFα. HMEC were grown in culture medium for 24 hours and additionally incubated in medium (basal) for different time intervals (6, 12, 24 hours) or grown in culture medium for 24 hours and additionally incubated with TNFα (TNFα) for different time intervals (6, 12, 24 hours) or incubated with poly (I:C) for 24 hours and then grown in medium (poly (I:C)) or stimulated with TNFα (poly (I:C) + TNFα) for different time intervals (6, 12, 24 hours). mRNA expression of selected cytokines and chemokines IL-6 (A), IL-8 (C), IP-10 (E), RANTES (G), MCP-1 (H), IFN-β (I), MCSF (J), <t>ICAM-1</t> (K) and VCAM-1 (L) was analyzed by RT-PCR. Protein synthesis of selected targets IL-6 (B), IL-8 (D) and IP-10 (F) was also confirmed by ELISA. Results are given as means ± SD of three experiments done in parallel for each condition and rRNA served as the reference gene. Comparable results were obtained in two series of independent experiments. Statistically significant differences to the control are depicted with * = p≤0.05, ** = p≤0.01.
    Gene Exp Icam1 Hs00164932 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 355 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher gene exp icam1 mm00516023 m1
    Effect of fullerenol on the relative gene expression levels of adhesion molecules in mouse brain microvascular endothelial cell (MBMEC) cultures under basal and inflammatory conditions. Real time PCR analysis of the expression levels of <t>ICAM-1</t> ( A ) and VCAM-1 ( B ) in MBMEC after exposure to interferon-γ and tumor necrosis factor-α (inflamed; I + T; 100 IU each) and treatment with fullerenol (F; 1, 10 and 100 µg/mL; n = 4) for 18 h compared to cultures under basal (homeostatic milieu) conditions. GAPDH was used as a housekeeping gene. Ctrl, untreated control; Veh, vehicle treatment.
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    92
    Leinco Technologies icam 1
    Brefeldin A, but not 1-deoxymannojirimycin, inhibits IL-1α-induced cell-surface <t>ICAM-1</t> expression. A549 cells were preincubated with various concentrations of 1-deoxymannojirimycin (A) or brefeldin A (B) for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P
    Icam 1, supplied by Leinco Technologies, used in various techniques. Bioz Stars score: 92/100, based on 66 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Pharmingen icam 1
    Expression of pCICAM-1 and pCLFA-3 on human rhabdomyosarcoma ( RD ) cells in vitro . RD cells were transfected with pCDNA3 (control), pCICAM-1, or pCLFA-3. Three days after transfection, the cells were removed from the plates and were analyzed by FACS ® analysis using either control antibodies, α–intracellular adhesion molecule-1 ( <t>ICAM-1</t> ), or α–lymphocyte function associated-3 ( LFA-3 ) antibodies to detect expression of the transfected gene product.
    Icam 1, supplied by Pharmingen, used in various techniques. Bioz Stars score: 92/100, based on 192 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    98
    Abcam anti icam 1
    <t>ICAM-1</t> expression in aorta after 12 weeks. A: Immunohistochemistry analyses of ICAM-1 in aorta (The arrows indicate positive expressions). B: Mean optical density values of ICAM-1. The optical density of ICAM-1 were quantitatively analyzed with Image - Pro Plus after 12 weeks. C: control, standard diet for 12 weeks ( n = 5); H: high-cholesterol diet for 12 weeks ( n = 5); HO: high-cholesterol diet with ogi for 12 weeks ( n = 5); HOH: high-cholesterol diet with ogi and hesperidin for 12 weeks ( n = 5); HOG: high-cholesterol diet with ogi and ginger for 12 weeks ( n = 5); HE: high-cholesterol diet with ezetimibe for 12 weeks ( n = 5). * P
    Anti Icam 1, supplied by Abcam, used in various techniques. Bioz Stars score: 98/100, based on 256 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Dianova icam 1
    Graphics and histograms (cytoflow data) of the effect of MMF (50, 100, 150, 200, 250, and 300 μg/mL) on TNF-α-induced expression of <t>ICAM-1</t> in HCAECs (A, B) and HCMSMCs (C, D) after 18 h. Negative control (dotted line) and ICAM-1 expression in untreated cells (grey line) are included.
    Icam 1, supplied by Dianova, used in various techniques. Bioz Stars score: 92/100, based on 86 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher anti icam 1
    TCR-mediated absorption of membrane vesicles. ( a ) Absorption of B7-1 by purified naïve or activated CD8 + 2C cells after incubation for 1 h with L d .B7-1 or L d <t>.B7-1.ICAM-1</t> Dros APCs loaded with QL9 peptide at 10 μM; activated T cells were prepared by preculturing cells for 12 h with PMA plus ionomycin. T cells and APCs were either cultured together (intact APCs) or separated from each other by placing APCs in a transwell (pore size 3 μm); Dros cells are large ( > 20 μm) and were unable to pass through the Transwell membrane. After culture, T cells were stained for B7-1, L d , and CD8 and then examined by flow cytometry. The data show staining of gated CD8 + cells. ( a Upper ) B7-1 staining of resting vs. activated 2C cells after culture with L d .B7-1 vs. L d .B7-1.ICAM-1 Dros APCs. ( a Lower ) B7-1 and L d staining of activated 2C cells cultured with L d .B7-1.ICAM-1 Dros APCs in the absence or presence of anti-LFA-1 mAb (5 ng/ml). ( b ) Morphology of membrane vesicles. Culture supernatants from L d .B7-1.ICAM-1 Dros APCs were depleted of cell debris, then ultracentrifuged. ( Left ) Electron microscopic view of pelleted material is shown at low ( Upper ) and high ( Lower ) magnification. (Bar, 200 nm.) Much of the material in the pellet shows the morphology of membrane vesicles; cell debris, more prominent in other fields, is also present. ( Right ) Electron microscopic view of magnetic beads that were coated with anti-ICAM-1 mAb ( Lower ) or an Ig isotype-matched control mAb ( Upper ) before incubation with the above membrane vesicles.
    Anti Icam 1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 166 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Becton Dickinson anti icam 1
    Pearson's correlation analysis between the mean value of <t>ICAM-1</t> and NF-κB expression in the 4 treatment groups. ICAM, intercellular adhesion molecule; NF, nuclear factor.
    Anti Icam 1, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 93/100, based on 320 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    USCN Life icam 1
    AS-IV decreased the serum levels of TNF- α , MCP-1, and <t>ICAM-1</t> in rats with ischemic AKI. Serum levels of TNF- α (a), MCP-1 (b), and ICAM-1 (c) in sham, vehicle-, or AS-IV-pretreated rats at 12 h of reperfusion. Serum levels of TNF- α (d), MCP-1 (e), and ICAM-1 (f) in sham, vehicle-, or AS-IV-pretreated rats at 24 h of reperfusion. Results are expressed as mean ± SD ( n = 8). * P
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    Bender MedSystems icam 1
    Adhesion of (a) CS2 IE and (b) CS2KO9 IE to immobilized receptors, expressed as IE bound/mm 2 . Data shown are the mean + SEM of two or more independent experiments, performed in triplicate. CSA, chondroitin sulphate A; CSA+10 μg/ml, Adhesion to CSA in presence of free CSA at 10 μg/ml; HCSPG, human chondroitin sulphate proteoglycan; <t>ICAM-1,</t> intercellular adhesion molecule 1. HA, hyaluronic acid; FG, fibrinogen.
    Icam 1, supplied by Bender MedSystems, used in various techniques. Bioz Stars score: 92/100, based on 68 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Bio-Rad icam 1
    Effect of Pom on MHC-I (HLA-A, B and C), ICAM and B7-2 mRNA gene expression in BCBL-1 cells induced with butyrate BCBL-1 cells were treated with control (DMSO) or Pom (1 μM) for 24 h followed by treatment with PBS or butyrate for an additional 24 h. Total mRNA was isolated and analyzed for expression levels by real time QT-PCR and was normalized to 18S levels. Shown are the fold changes in mRNA expression for total A . HLA and HLA A, B and C alleles following treatment and B . <t>ICAM-1</t> and B7-2. Values are the average +/- standard deviation of four independent experiments. *** P
    Icam 1, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 92/100, based on 395 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    96
    R&D Systems mouse icam 1 cd54 antibody
    Effect of Pom on MHC-I (HLA-A, B and C), ICAM and B7-2 mRNA gene expression in BCBL-1 cells induced with butyrate BCBL-1 cells were treated with control (DMSO) or Pom (1 μM) for 24 h followed by treatment with PBS or butyrate for an additional 24 h. Total mRNA was isolated and analyzed for expression levels by real time QT-PCR and was normalized to 18S levels. Shown are the fold changes in mRNA expression for total A . HLA and HLA A, B and C alleles following treatment and B . <t>ICAM-1</t> and B7-2. Values are the average +/- standard deviation of four independent experiments. *** P
    Mouse Icam 1 Cd54 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 151 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam anti icam 1 antibody
    Increased inflammation, ER stress and oxidative stress in aorta of ApoCIIItgLDLR−/− mice comparing to LDLR−/− mice. ( a ) Representative images of Oil Red O (ORO) stained aortic roots and immunohistochemical staining of aortic sinus sections of Mac2, 4HNE and VCAM-1 expression in LDLR−/− and ApoCIIItgLDLR−/− mice. ( b ) Representative Western blot images of VCAM-1 and <t>ICAM-1</t> protein expression in aortas of LDLR−/− and ApoCIIItgLDLR−/− mice and the protein quantification by densitometry ( n = 4). ( c ) Representative Western blot images of GRP78 protein expression in aortas of LDLR−/− and ApoCIIItgLDLR−/− mice and the protein quantification by densitometry ( n = 4). Values are expressed as mean ± SEM, * p
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    94
    Thermo Fisher cd54
    Human CMV infection alters the cell surface expression of key molecules involved in mDC function. (A) Dot plot showing expression of MHC class I molecules on the surface of mock infected (left) or CMV strain TB40/E-infected LC-derived mDCs (right) at day 2 p.i. Cells were stained with a PE-conjugated anti-MHC class I monoclonal antibody ( x axis), as well as with an FITC-conjugated anti-IE1/IE2 monoclonal antibody ( y axis). (B) Flow cytometry analysis of expression levels of MHC class I, MHC class II, CD1a, CD80, CD86, CD83, <t>CD54,</t> CCR7, and CD40 on the surface of mock-infected and CMV strain TB40/E-infected LC-derived mDCs at day 2 p.i. Filled histograms, mock-infected cells; open histograms, TB40/E-infected cells; gray line, isotype controls.
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    R&D Systems recombinant human icam 1
    Dynamic analysis of cytoadherence features of eight isolates during the adaptive cultivation. Significant binding was defined as > 5PRBC/mm2, and the final value of bound cells numbers was adjusted in terms of parasitemia of different batches used in the assay. The four purified receptors, CD36, <t>ICAM-1,</t> CSA, and HA were used as immobilized receptors with BSA as negative control. The time points of upregulation of ICAM-1 binding activity were indicated by arrows.
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    Image Search Results


    Effects of SsnB on the LPS-induced ICAM-1 and VCAM-1 expression in HUVECs. Cells were treated with SsnB and LPS as indicated for 24 h, were then lysed, and the protein levels were detected by Western blot analysis ( upper ). The blots were quantified by

    Journal: Archives of pharmacal research

    Article Title: Sparstolonin B suppresses lipopolysaccharide-induced inflammation in human umbilical vein endothelial cells

    doi: 10.1007/s12272-013-0120-8

    Figure Lengend Snippet: Effects of SsnB on the LPS-induced ICAM-1 and VCAM-1 expression in HUVECs. Cells were treated with SsnB and LPS as indicated for 24 h, were then lysed, and the protein levels were detected by Western blot analysis ( upper ). The blots were quantified by

    Article Snippet: Mouse monoclonal antibody to ICAM-1 was obtained from Zymed Laboratories Inc (San Francisco, CA).

    Techniques: Expressing, Western Blot

    Effect of APC on the HMGB1-mediated expression of cell adhesion molecules in HUVECs. Confluent HUVECs were incubated with HMGB1 (1 μg/mL for 16 hours) after treating cells with indicated concentrations of APC for 3 hours. The cell surface expression of VCAM-1 (A), ICAM-1 (B), and E-selectin (C) on HUVECs was measured by a cell-based ELISA as described in “Methods.” All results are shown as means ± SDs of 5 different experiments. * P

    Journal: Blood

    Article Title: Activated protein C inhibits high mobility group box 1 signaling in endothelial cells

    doi: 10.1182/blood-2011-06-360701

    Figure Lengend Snippet: Effect of APC on the HMGB1-mediated expression of cell adhesion molecules in HUVECs. Confluent HUVECs were incubated with HMGB1 (1 μg/mL for 16 hours) after treating cells with indicated concentrations of APC for 3 hours. The cell surface expression of VCAM-1 (A), ICAM-1 (B), and E-selectin (C) on HUVECs was measured by a cell-based ELISA as described in “Methods.” All results are shown as means ± SDs of 5 different experiments. * P

    Article Snippet: After washing 3 times, mouse anti–human mAbs to VCAM-1, ICAM-1, and E-selectin (Chemicon International) were added.

    Techniques: Expressing, Incubation, In-Cell ELISA

    Effect of APC on the LPS-mediated expression of cell adhesion molecules in HUVECs. Confluent HUVECs were incubated with LPS (100 ng/mL for 4 hours) after treating cells with indicated concentrations of APC for 3 hours. The cell surface expression of VCAM-1 (A), ICAM-1 (B), and E-selectin (C) on HUVECs was measured by a cell-based ELISA as described in “Methods.” All results are shown as means ± SDs of 2 different experiments with triplicate wells. * P

    Journal: Blood

    Article Title: Activated protein C inhibits high mobility group box 1 signaling in endothelial cells

    doi: 10.1182/blood-2011-06-360701

    Figure Lengend Snippet: Effect of APC on the LPS-mediated expression of cell adhesion molecules in HUVECs. Confluent HUVECs were incubated with LPS (100 ng/mL for 4 hours) after treating cells with indicated concentrations of APC for 3 hours. The cell surface expression of VCAM-1 (A), ICAM-1 (B), and E-selectin (C) on HUVECs was measured by a cell-based ELISA as described in “Methods.” All results are shown as means ± SDs of 2 different experiments with triplicate wells. * P

    Article Snippet: After washing 3 times, mouse anti–human mAbs to VCAM-1, ICAM-1, and E-selectin (Chemicon International) were added.

    Techniques: Expressing, Incubation, In-Cell ELISA

    Effect of DYSGT on ET-1, ICAM-1, and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis

    doi: 10.1155/2013/783576

    Figure Lengend Snippet: Effect of DYSGT on ET-1, ICAM-1, and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P

    Article Snippet: Similarly, in WTD-fed ApoE KO mice, immunofluorescence of the aorta tissues showed that ICAM-1 and ET-1 expression were decreased in rosiglitazone and DYSGT groups compared with ApoE KO group ( ).

    Techniques: Expressing, Mouse Assay, Western Blot

    Immunofluorescence staining of (a) ICAM-1 and (b) ET-1 in the aorta. Representative histological sections are thoracic aorta of Cont., ApoE KO mice, ApoE mice treated with rosiglitazone, and ApoE mice treated with DYSGT incubated with anti-ICAM-1, anti-ET-1 antibodies, respectively. Original magnification: 100x.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis

    doi: 10.1155/2013/783576

    Figure Lengend Snippet: Immunofluorescence staining of (a) ICAM-1 and (b) ET-1 in the aorta. Representative histological sections are thoracic aorta of Cont., ApoE KO mice, ApoE mice treated with rosiglitazone, and ApoE mice treated with DYSGT incubated with anti-ICAM-1, anti-ET-1 antibodies, respectively. Original magnification: 100x.

    Article Snippet: Similarly, in WTD-fed ApoE KO mice, immunofluorescence of the aorta tissues showed that ICAM-1 and ET-1 expression were decreased in rosiglitazone and DYSGT groups compared with ApoE KO group ( ).

    Techniques: Immunofluorescence, Staining, Mouse Assay, Incubation

    (A) detection of neutrophils by chloroacetate esterase staining in liver tissues. Arrow: positive stained neutrophils. m: mouse age in months. OVE: OVE26. (B) Western blot analysis of proinflammatory cytokines (TGFβ, TNFα, ICAM1, and CTGF) in the liver tissues from OVE26 mice as well as the FVB controls. Data are presented as mean ± SD. * P

    Journal: International Journal of Biological Sciences

    Article Title: ER Stress and Autophagy Dysfunction Contribute to Fatty Liver in Diabetic Mice

    doi: 10.7150/ijbs.10690

    Figure Lengend Snippet: (A) detection of neutrophils by chloroacetate esterase staining in liver tissues. Arrow: positive stained neutrophils. m: mouse age in months. OVE: OVE26. (B) Western blot analysis of proinflammatory cytokines (TGFβ, TNFα, ICAM1, and CTGF) in the liver tissues from OVE26 mice as well as the FVB controls. Data are presented as mean ± SD. * P

    Article Snippet: The primary antibodies were used including the antibodies against TGFβ, TNFα, ICAM1, CTGF, GRP78, ATF6, CCAAT/enhancer-binding protein-homologous protein (CHOP) caspase-12, (Santa Cruz Biotechnology, Santa Cruz, CA), microtubule-associated protein 1 light-chain 3(LC3) BII, P62, p70 S6 Kinase (for total p70 S6 kinase protein detection), Phospho-p70 S6 Kinase, caspase-8, Bax and Bcl-2 (Cell Signaling Technology).

    Techniques: Staining, Western Blot, Mouse Assay

    RAS inhibitor attenuated the H 2 O 2 -induced increases in expressions of p53, ICAM-1, p-eNOS, p-AKT and p-mTOR via AKT/mTOR pathway. A – HCAECs were pre-treated with captopril or combined with AKT inhibitor or activator, then exposed to H 2 O 2 for 48 h. Cell lysate was analyzed for p53, ICAM-1, p-eNOS, p-Akt and p-mTOR protein levels by immunoblotting. B – Shows a column bar graph analysis *p

    Journal: Archives of Medical Science : AMS

    Article Title: Renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway

    doi: 10.5114/aoms.2018.74026

    Figure Lengend Snippet: RAS inhibitor attenuated the H 2 O 2 -induced increases in expressions of p53, ICAM-1, p-eNOS, p-AKT and p-mTOR via AKT/mTOR pathway. A – HCAECs were pre-treated with captopril or combined with AKT inhibitor or activator, then exposed to H 2 O 2 for 48 h. Cell lysate was analyzed for p53, ICAM-1, p-eNOS, p-Akt and p-mTOR protein levels by immunoblotting. B – Shows a column bar graph analysis *p

    Article Snippet: After incubation in blocking solution (4% nonfat milk, Sigma), the membranes were probed overnight with 1 : 2000 dilution primary antibody (monoclonal antibody to p53 (Abcam, USA), ICAM-1 (Abcam, USA), p-Akt (Cell Signaling Technology, USA), p-eNOS (Santa Cruz Biotechnology, USA), p-mTOR (Cell Signaling Technology, USA) and β-actin (Abcam, USA)).

    Techniques:

    MiR-19b-3p/NRP1 axis regulates epithelial-mesenchymal transition and focal adhesion in GC cells. a SGC-7901 cells were transfected with mimic negative control, miR-19b-3p mimics, pcDNA-3.1-NRP1 overexpression vector or negative control pcDNA3.1 vector. The protein expression of NRP1, E-cadherin, vimentin, N-cadherin, BMP4, ICAM1, and VCAM1 was analyzed by western blot 48 h later. b SGC-7901 cells were transfected with inhibitor negative control, miR-19b-3p inhibitor, si-NRP1 or negative control si-NC. The protein expression of NRP1, E-cadherin, vimentin, N-cadherin, BMP4, ICAM1, and VCAM1 was analyzed by western blot 48 h later. GAPDH was used as an internal loading control

    Journal: Cancer Cell International

    Article Title: MicroRNA-19b-3p suppresses gastric cancer development by negatively regulating neuropilin-1

    doi: 10.1186/s12935-020-01257-0

    Figure Lengend Snippet: MiR-19b-3p/NRP1 axis regulates epithelial-mesenchymal transition and focal adhesion in GC cells. a SGC-7901 cells were transfected with mimic negative control, miR-19b-3p mimics, pcDNA-3.1-NRP1 overexpression vector or negative control pcDNA3.1 vector. The protein expression of NRP1, E-cadherin, vimentin, N-cadherin, BMP4, ICAM1, and VCAM1 was analyzed by western blot 48 h later. b SGC-7901 cells were transfected with inhibitor negative control, miR-19b-3p inhibitor, si-NRP1 or negative control si-NC. The protein expression of NRP1, E-cadherin, vimentin, N-cadherin, BMP4, ICAM1, and VCAM1 was analyzed by western blot 48 h later. GAPDH was used as an internal loading control

    Article Snippet: The primary antibodies used in the study were listed as following: Ki-67 (Proteintech, 27309-1-AP), NRP1 (Abcam, ab81321), E-cadherin (Abcam, ab194982), vimentin (Abcam, ab92547), N-cadherin (Abcam, ab18203), BMP4 (Abcam, ab200796), ICAM1 (Abcam, ab221777), VCAM1 (Abcam, ab134047).

    Techniques: Transfection, Negative Control, Over Expression, Plasmid Preparation, Expressing, Western Blot

    MiR-19b-3p/NRP1 axis regulates epithelial-mesenchymal transition and focal adhesion in GC. a GSVA analysis the different regulated signaling pathways in GC tumor compared with adjacent non-tumor tissues. b , c GSEA analysis the enrichment of signature genes in NRP1 high or low group. d IHC staining of E-cadherin, vimentin, and N-cadherin in xenograft tumor tissues from NC or sh-NRP1 group. Scale bars, 200 μm. e IHC staining of BMP4, ICAM1, and VCAM1 in xenograft tumor tissues from NC or sh-NRP1 group. * p

    Journal: Cancer Cell International

    Article Title: MicroRNA-19b-3p suppresses gastric cancer development by negatively regulating neuropilin-1

    doi: 10.1186/s12935-020-01257-0

    Figure Lengend Snippet: MiR-19b-3p/NRP1 axis regulates epithelial-mesenchymal transition and focal adhesion in GC. a GSVA analysis the different regulated signaling pathways in GC tumor compared with adjacent non-tumor tissues. b , c GSEA analysis the enrichment of signature genes in NRP1 high or low group. d IHC staining of E-cadherin, vimentin, and N-cadherin in xenograft tumor tissues from NC or sh-NRP1 group. Scale bars, 200 μm. e IHC staining of BMP4, ICAM1, and VCAM1 in xenograft tumor tissues from NC or sh-NRP1 group. * p

    Article Snippet: The primary antibodies used in the study were listed as following: Ki-67 (Proteintech, 27309-1-AP), NRP1 (Abcam, ab81321), E-cadherin (Abcam, ab194982), vimentin (Abcam, ab92547), N-cadherin (Abcam, ab18203), BMP4 (Abcam, ab200796), ICAM1 (Abcam, ab221777), VCAM1 (Abcam, ab134047).

    Techniques: Immunohistochemistry, Staining

    ICAM-1 and CD11c co-localize during exosome-macrophage interactions. (A) Immunoblotting analysis reveals exosomes from the pancreatic cancer cell lines AsPC-1 and BxPC-3 are enriched in the surface-exposed proteins ICAM-1 and EpCAM, while CD9 is more broadly expressed. The pan-exosomal marker flotillin-1 is used as a loading control. (B) Co-localization of exosome proteins and macrophage proteins is demonstrated by immunostaining for the exosome marker ICAM-1 (green, panel 1) or the macrophage marker CD11c (red, panel 2) after mixing AsPC-1 exosomes with THP-1-derived, non-polarized macrophages. Panel 3 is a merged image showing co-localization of ICAM-1 and CD11c staining (yellow, indicated by an arrow), and is suggestive of ICAM-1 and CD11c protein-protein interaction. THP-1-derived macrophages not mixed with exosomes (cells only) show little ICAM-1 staining (green, panel 4), suggesting exosomes were the main source of the ICAM-1 signal. In the absence of exosomes, more CD11c is associated with the THP-1 cell surface (red, panel 5), and merged images of THP-1 only staining show few areas of signal co-localization (panel 6, yellow). Scale bar = 3.0 μm (C) Quantitation of ICAM-1:CD11c co-localized signal in THP-1 cells mixed with AsPC-1 exosomes or in THP-1 cells alone. *** p

    Journal: PLoS ONE

    Article Title: Tumor-promoting effects of pancreatic cancer cell exosomes on THP-1-derived macrophages

    doi: 10.1371/journal.pone.0206759

    Figure Lengend Snippet: ICAM-1 and CD11c co-localize during exosome-macrophage interactions. (A) Immunoblotting analysis reveals exosomes from the pancreatic cancer cell lines AsPC-1 and BxPC-3 are enriched in the surface-exposed proteins ICAM-1 and EpCAM, while CD9 is more broadly expressed. The pan-exosomal marker flotillin-1 is used as a loading control. (B) Co-localization of exosome proteins and macrophage proteins is demonstrated by immunostaining for the exosome marker ICAM-1 (green, panel 1) or the macrophage marker CD11c (red, panel 2) after mixing AsPC-1 exosomes with THP-1-derived, non-polarized macrophages. Panel 3 is a merged image showing co-localization of ICAM-1 and CD11c staining (yellow, indicated by an arrow), and is suggestive of ICAM-1 and CD11c protein-protein interaction. THP-1-derived macrophages not mixed with exosomes (cells only) show little ICAM-1 staining (green, panel 4), suggesting exosomes were the main source of the ICAM-1 signal. In the absence of exosomes, more CD11c is associated with the THP-1 cell surface (red, panel 5), and merged images of THP-1 only staining show few areas of signal co-localization (panel 6, yellow). Scale bar = 3.0 μm (C) Quantitation of ICAM-1:CD11c co-localized signal in THP-1 cells mixed with AsPC-1 exosomes or in THP-1 cells alone. *** p

    Article Snippet: When only THP-1-derived macrophages (no exosomes) were visualized, little ICAM-1 signal was observed, suggesting that the ICAM-1 was mainly associated with the AsPC-1 exosomes and not with the THP-1 macrophages, and the CD11c signal remained at the cell surface.

    Techniques: Marker, Immunostaining, Derivative Assay, Staining, Quantitation Assay

    CMH suppresses endothelial VCAM-1 and ICAM-1 expression during EAE. a and c . Frozen sections of lumbar spinal cord taken from disease-free, EAE-normoxia or EAE-CMH mice at the peak symptomatic phase of EAE were stained for CD31 (AlexaFluor-488) and VCAM-1 (Cy-3) in panel A or CD31 (Cy-3) and ICAM-1 (AlexaFluor-488) in panel C. Scale bar = 100 μm (inset, scale bar = 50 μm). b and d . Quantification of VCAM-1 ( b ) and ICAM-1 expression ( d ). Results are expressed as the mean ± SEM ( n = 6 mice/group). Note that CMH markedly suppressed vascular expression of VCAM-1 and ICAM-1. ** p

    Journal: Acta Neuropathologica Communications

    Article Title: Hypoxic pre-conditioning suppresses experimental autoimmune encephalomyelitis by modifying multiple properties of blood vessels

    doi: 10.1186/s40478-018-0590-5

    Figure Lengend Snippet: CMH suppresses endothelial VCAM-1 and ICAM-1 expression during EAE. a and c . Frozen sections of lumbar spinal cord taken from disease-free, EAE-normoxia or EAE-CMH mice at the peak symptomatic phase of EAE were stained for CD31 (AlexaFluor-488) and VCAM-1 (Cy-3) in panel A or CD31 (Cy-3) and ICAM-1 (AlexaFluor-488) in panel C. Scale bar = 100 μm (inset, scale bar = 50 μm). b and d . Quantification of VCAM-1 ( b ) and ICAM-1 expression ( d ). Results are expressed as the mean ± SEM ( n = 6 mice/group). Note that CMH markedly suppressed vascular expression of VCAM-1 and ICAM-1. ** p

    Article Snippet: Hamster monoclonal antibodies used included CD31 (clone 2H8) from Abcam (Cambridge, MA) and ICAM-1 (clone 3E2) from BD Pharmingen.

    Techniques: Expressing, Mouse Assay, Staining

    Analysis of the miR-124 promoter and transcription factor Sp1 binds to miR-124 promoter (A) RAW264.7 cells were co-transfected with pRL-TK and a miR-124 promoter reporter plasmid containing various lengths of the miR-124 promoter. The first nucleotide of mature pre-miR-124 is assigned +1. Right panel shows the relative luciferase activities of these plasmids. Luciferase activity of the mock transfected empty vector pGL3-Basic was used for normalization. The data in graph were shown in mean ± SEM of 3 different transfections. (B) Schematic diagram of miR-124 genomic location in mouse chromosome 2. The promoter region from pre-197 to pre-27 was used for analysis of potential transcription factor binding sites. Two Sp1 binding sites are indicated as diamonds. The sequences of mutated sites are shown under the locus diagram. (C) Schematic representation of deletion mutants 1 and 2 in the full-length miR-124 promoter. (D) RAW264.7 cells were co-transfected with the above promoter reporter constructs and pRL-TK. Post-transfection for 36h, samples were collected and analyzed for dual luciferase activity. (E) Real-time qPCR and Western blot analysis of the expression of Sp1 after transfection with ICAM-1 siRNA and negative control. ( * p

    Journal: Oncotarget

    Article Title: ICAM-1 regulates macrophage polarization by suppressing MCP-1 expression via miR-124 upregulation

    doi: 10.18632/oncotarget.22948

    Figure Lengend Snippet: Analysis of the miR-124 promoter and transcription factor Sp1 binds to miR-124 promoter (A) RAW264.7 cells were co-transfected with pRL-TK and a miR-124 promoter reporter plasmid containing various lengths of the miR-124 promoter. The first nucleotide of mature pre-miR-124 is assigned +1. Right panel shows the relative luciferase activities of these plasmids. Luciferase activity of the mock transfected empty vector pGL3-Basic was used for normalization. The data in graph were shown in mean ± SEM of 3 different transfections. (B) Schematic diagram of miR-124 genomic location in mouse chromosome 2. The promoter region from pre-197 to pre-27 was used for analysis of potential transcription factor binding sites. Two Sp1 binding sites are indicated as diamonds. The sequences of mutated sites are shown under the locus diagram. (C) Schematic representation of deletion mutants 1 and 2 in the full-length miR-124 promoter. (D) RAW264.7 cells were co-transfected with the above promoter reporter constructs and pRL-TK. Post-transfection for 36h, samples were collected and analyzed for dual luciferase activity. (E) Real-time qPCR and Western blot analysis of the expression of Sp1 after transfection with ICAM-1 siRNA and negative control. ( * p

    Article Snippet: The commercial of ICAM-1 siRNA (sc-29355), antibodies ICAM-1 and MCP-1 were purchased from Santa Cruz.

    Techniques: Transfection, Plasmid Preparation, Luciferase, Activity Assay, Binding Assay, Construct, Real-time Polymerase Chain Reaction, Western Blot, Expressing, Negative Control

    In primary macrophages confirm ICAM-1 regulation of MCP-1 expression via miR124 (A) Real-time qPCR analysis of expression levels of miR-124 in porcine alveolar macrophages (primary macrophages) after transfected with mimic-NC, miR-124 mimics, inhibitor-NC and miR-124 inhibitor. (B) PAM cells were transfected with miR-124 mimic or mimic control, inhibitor-NC or miR-124 inhibitor for 48h, MCP-1 protein levels were measured with Western blotting. (C) In PAM cells transfected with siRNA-ICAM-1, knockdown of ICAM-1 was measured with Western blot. (D) Real-time qPCR and Western blot analysis of the expression of Sp1 after transfection with ICAM-1 siRNA and negative control. (E) The mRNA expressions of M1 and M2 markers in PAM cells transfected with siRNA-ICAM-1 or miR-124 mimics for 24h. ( * p

    Journal: Oncotarget

    Article Title: ICAM-1 regulates macrophage polarization by suppressing MCP-1 expression via miR-124 upregulation

    doi: 10.18632/oncotarget.22948

    Figure Lengend Snippet: In primary macrophages confirm ICAM-1 regulation of MCP-1 expression via miR124 (A) Real-time qPCR analysis of expression levels of miR-124 in porcine alveolar macrophages (primary macrophages) after transfected with mimic-NC, miR-124 mimics, inhibitor-NC and miR-124 inhibitor. (B) PAM cells were transfected with miR-124 mimic or mimic control, inhibitor-NC or miR-124 inhibitor for 48h, MCP-1 protein levels were measured with Western blotting. (C) In PAM cells transfected with siRNA-ICAM-1, knockdown of ICAM-1 was measured with Western blot. (D) Real-time qPCR and Western blot analysis of the expression of Sp1 after transfection with ICAM-1 siRNA and negative control. (E) The mRNA expressions of M1 and M2 markers in PAM cells transfected with siRNA-ICAM-1 or miR-124 mimics for 24h. ( * p

    Article Snippet: The commercial of ICAM-1 siRNA (sc-29355), antibodies ICAM-1 and MCP-1 were purchased from Santa Cruz.

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Transfection, Western Blot, Negative Control

    Different miRNA profiles of ICAM-1 -/- mouse lungs and wild-type mouse lungs (A) Differential expression of known mouse miRNAs in scatter plot. MiRNA profiles in wild-type mouse lungs are distinguished from that in ICAM-1 -/- mouse lungs in Table 2 . (B) and (C) Validation of selected microRNA sequence data by real-time qPCR. The relative amounts of each miRNA were normalized to U6 snRNA. (D) Analysis of miR-124 relative expression in the wild type mouse tissues by real-time qPCR. The data in graph were shown in mean ± SEM of 3 mice.

    Journal: Oncotarget

    Article Title: ICAM-1 regulates macrophage polarization by suppressing MCP-1 expression via miR-124 upregulation

    doi: 10.18632/oncotarget.22948

    Figure Lengend Snippet: Different miRNA profiles of ICAM-1 -/- mouse lungs and wild-type mouse lungs (A) Differential expression of known mouse miRNAs in scatter plot. MiRNA profiles in wild-type mouse lungs are distinguished from that in ICAM-1 -/- mouse lungs in Table 2 . (B) and (C) Validation of selected microRNA sequence data by real-time qPCR. The relative amounts of each miRNA were normalized to U6 snRNA. (D) Analysis of miR-124 relative expression in the wild type mouse tissues by real-time qPCR. The data in graph were shown in mean ± SEM of 3 mice.

    Article Snippet: The commercial of ICAM-1 siRNA (sc-29355), antibodies ICAM-1 and MCP-1 were purchased from Santa Cruz.

    Techniques: Expressing, Sequencing, Real-time Polymerase Chain Reaction, Mouse Assay

    ICAM-1depletion attenuates miR-124 expression and promotes MCP-1 production in macrophages Downregulation of miR-124 (A) and upregulation of MCP-1 (B) in RAW264.7 cells transfected with siRNA against ICAM-1. Twenty-four h after transfection, expressions were measured with real-time qPCR. The data in graph were shown in mean ± SEM of 3 different transfections. (C) MCP-1 protein levels were upregulated when ICAM-1 was downregulated. RAW264.7 cells were co-transfected with siRNA-ICAM-1 and miR-124 mimics, MCP-1 protein levels were measured with Western blot analysis 48h later. (D) MCP-1 protein expression was determined by ELISA. ( ** p

    Journal: Oncotarget

    Article Title: ICAM-1 regulates macrophage polarization by suppressing MCP-1 expression via miR-124 upregulation

    doi: 10.18632/oncotarget.22948

    Figure Lengend Snippet: ICAM-1depletion attenuates miR-124 expression and promotes MCP-1 production in macrophages Downregulation of miR-124 (A) and upregulation of MCP-1 (B) in RAW264.7 cells transfected with siRNA against ICAM-1. Twenty-four h after transfection, expressions were measured with real-time qPCR. The data in graph were shown in mean ± SEM of 3 different transfections. (C) MCP-1 protein levels were upregulated when ICAM-1 was downregulated. RAW264.7 cells were co-transfected with siRNA-ICAM-1 and miR-124 mimics, MCP-1 protein levels were measured with Western blot analysis 48h later. (D) MCP-1 protein expression was determined by ELISA. ( ** p

    Article Snippet: The commercial of ICAM-1 siRNA (sc-29355), antibodies ICAM-1 and MCP-1 were purchased from Santa Cruz.

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

    ICAM-1 and miR-124 induce different macrophage polarizations (A) Real-time qPCR analysis of the mRNA expression of M1 marker (iNOS, CD86, IL-6) and M2 (ym-1, Mrc-1, IL-10) markers in ICAM-1 siRNA or negative control transfected with RAW264.7 cells. RAW264.7 cells treated with for 24h. (B) RAW264.7 cells were transfected with miR-124 mimics or negative control, LPS (2ug/ml) or IL-4 (20ng/ml), mRNA expressions of M1 and M2 markers were analyzed with real-time qPCR. (C) The mRNA expressions of M1 and M2 markers in RAW264.7 cells transfected with siRNA-ICAM-1 for 24h in the presence or absence of IL-4. (D) The mRNA expressions of M1 and M2 markers in RAW264.7 cells transfected with miR-124 mimics for 24h in the presence or absence of LPS. ( * p

    Journal: Oncotarget

    Article Title: ICAM-1 regulates macrophage polarization by suppressing MCP-1 expression via miR-124 upregulation

    doi: 10.18632/oncotarget.22948

    Figure Lengend Snippet: ICAM-1 and miR-124 induce different macrophage polarizations (A) Real-time qPCR analysis of the mRNA expression of M1 marker (iNOS, CD86, IL-6) and M2 (ym-1, Mrc-1, IL-10) markers in ICAM-1 siRNA or negative control transfected with RAW264.7 cells. RAW264.7 cells treated with for 24h. (B) RAW264.7 cells were transfected with miR-124 mimics or negative control, LPS (2ug/ml) or IL-4 (20ng/ml), mRNA expressions of M1 and M2 markers were analyzed with real-time qPCR. (C) The mRNA expressions of M1 and M2 markers in RAW264.7 cells transfected with siRNA-ICAM-1 for 24h in the presence or absence of IL-4. (D) The mRNA expressions of M1 and M2 markers in RAW264.7 cells transfected with miR-124 mimics for 24h in the presence or absence of LPS. ( * p

    Article Snippet: The commercial of ICAM-1 siRNA (sc-29355), antibodies ICAM-1 and MCP-1 were purchased from Santa Cruz.

    Techniques: Real-time Polymerase Chain Reaction, Expressing, Marker, Negative Control, Transfection

    ICAM-1 deficiency or downregulation promotes MCP-1 expression in mouse lungs and macrophages (A) Comparison of MCP-1 expression in WT or ICAM-1 -/- mouse lungs by Western blot analysis. MCP-1 is elevated in ICAM-1 -/- mouse lungs. (B) Comparison of MCP-1 expression in WT or ICAM-1 -/- mouse heart and kidney. MCP-1 expression is relative decreased. (C) In RAW264.7 cells transfected with siRNA-ICAM-1, knockdown of ICAM-1 was measured with Western blot analysis. (D) In RAW264.7 transfected with siRNA-ICAM-1, MCP-1 expression is upregulated as measured with Western blot. ( ** p

    Journal: Oncotarget

    Article Title: ICAM-1 regulates macrophage polarization by suppressing MCP-1 expression via miR-124 upregulation

    doi: 10.18632/oncotarget.22948

    Figure Lengend Snippet: ICAM-1 deficiency or downregulation promotes MCP-1 expression in mouse lungs and macrophages (A) Comparison of MCP-1 expression in WT or ICAM-1 -/- mouse lungs by Western blot analysis. MCP-1 is elevated in ICAM-1 -/- mouse lungs. (B) Comparison of MCP-1 expression in WT or ICAM-1 -/- mouse heart and kidney. MCP-1 expression is relative decreased. (C) In RAW264.7 cells transfected with siRNA-ICAM-1, knockdown of ICAM-1 was measured with Western blot analysis. (D) In RAW264.7 transfected with siRNA-ICAM-1, MCP-1 expression is upregulated as measured with Western blot. ( ** p

    Article Snippet: The commercial of ICAM-1 siRNA (sc-29355), antibodies ICAM-1 and MCP-1 were purchased from Santa Cruz.

    Techniques: Expressing, Western Blot, Transfection

    NO-NIF improved endothelial dysfunction and renal tubular injury in DN. Immunoblotting (A) and immunohistochemistry (B and C) for ICAM-1 expression in the diabetic kidney of the C57BL/6 and KKAy mice with or without NO-NIF 4 weeks after the commencement of NO-NIF (30 mg/kg) administration. (A) Representative blot of ICAM-1 and β-actin. Equal amounts of protein in each sample were separated by SDS-PAGE and analysis for ICAM-1 by western blotting. (B) Representative immunohistochemical staining of ICAM-1 in glomeruli. (C) Quantitative analysis for staining of ICAM-1 in glomeruli. Values are expressed as the means ± S.E., n = 8–10. *p

    Journal: PLoS ONE

    Article Title: Nitrosonifedipine Ameliorates the Progression of Type 2 Diabetic Nephropathy by Exerting Antioxidative Effects

    doi: 10.1371/journal.pone.0086335

    Figure Lengend Snippet: NO-NIF improved endothelial dysfunction and renal tubular injury in DN. Immunoblotting (A) and immunohistochemistry (B and C) for ICAM-1 expression in the diabetic kidney of the C57BL/6 and KKAy mice with or without NO-NIF 4 weeks after the commencement of NO-NIF (30 mg/kg) administration. (A) Representative blot of ICAM-1 and β-actin. Equal amounts of protein in each sample were separated by SDS-PAGE and analysis for ICAM-1 by western blotting. (B) Representative immunohistochemical staining of ICAM-1 in glomeruli. (C) Quantitative analysis for staining of ICAM-1 in glomeruli. Values are expressed as the means ± S.E., n = 8–10. *p

    Article Snippet: The anti-ICAM-1 antibody was purchased from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA).

    Techniques: Immunohistochemistry, Expressing, Mouse Assay, SDS Page, Western Blot, Staining

    Amplification of poly (I:C)-mediated induction of cytokines, chemokines and adhesion molecules by TNFα. HMEC were grown in culture medium for 24 hours and additionally incubated in medium (basal) for different time intervals (6, 12, 24 hours) or grown in culture medium for 24 hours and additionally incubated with TNFα (TNFα) for different time intervals (6, 12, 24 hours) or incubated with poly (I:C) for 24 hours and then grown in medium (poly (I:C)) or stimulated with TNFα (poly (I:C) + TNFα) for different time intervals (6, 12, 24 hours). mRNA expression of selected cytokines and chemokines IL-6 (A), IL-8 (C), IP-10 (E), RANTES (G), MCP-1 (H), IFN-β (I), MCSF (J), ICAM-1 (K) and VCAM-1 (L) was analyzed by RT-PCR. Protein synthesis of selected targets IL-6 (B), IL-8 (D) and IP-10 (F) was also confirmed by ELISA. Results are given as means ± SD of three experiments done in parallel for each condition and rRNA served as the reference gene. Comparable results were obtained in two series of independent experiments. Statistically significant differences to the control are depicted with * = p≤0.05, ** = p≤0.01.

    Journal: PLoS ONE

    Article Title: Hepatitis C Virus Induced Endothelial Inflammatory Response Depends on the Functional Expression of TNFα Receptor Subtype 2

    doi: 10.1371/journal.pone.0113351

    Figure Lengend Snippet: Amplification of poly (I:C)-mediated induction of cytokines, chemokines and adhesion molecules by TNFα. HMEC were grown in culture medium for 24 hours and additionally incubated in medium (basal) for different time intervals (6, 12, 24 hours) or grown in culture medium for 24 hours and additionally incubated with TNFα (TNFα) for different time intervals (6, 12, 24 hours) or incubated with poly (I:C) for 24 hours and then grown in medium (poly (I:C)) or stimulated with TNFα (poly (I:C) + TNFα) for different time intervals (6, 12, 24 hours). mRNA expression of selected cytokines and chemokines IL-6 (A), IL-8 (C), IP-10 (E), RANTES (G), MCP-1 (H), IFN-β (I), MCSF (J), ICAM-1 (K) and VCAM-1 (L) was analyzed by RT-PCR. Protein synthesis of selected targets IL-6 (B), IL-8 (D) and IP-10 (F) was also confirmed by ELISA. Results are given as means ± SD of three experiments done in parallel for each condition and rRNA served as the reference gene. Comparable results were obtained in two series of independent experiments. Statistically significant differences to the control are depicted with * = p≤0.05, ** = p≤0.01.

    Article Snippet: Sequences were used as indicated or pre-developed Taq Man assay reagents or primers and probes were purchased from Applied Biosystems: NM_003265.2, HS00152933_m1 (human TLR3), NM_014314.3, Hs00204833_m1 (human RIG-I), NM_022168.2, Hs0170332_m1 (human MDA5), NM_000600.3, Hs00174131_m1 (human IL-6), NM_000584.2, Hs00174103_m1 (human IL-8), NM_002985.2, Hs00174575_m1 (human RANTES), NM_002982.3, Hs00234140_m1, (human MCP-1), NM_001565.2, Hs00171042_m1 (human IP-10), FP: CCT TCC TCC TGT CTG ATG GA ; RP: ACT GGT TGC CAT CAA ACT CC ; T1: 6FAM CAG ACA TGA CTT TGG ATT TCC CCA GG (human IFN-α), NM_002176.2, Hs00277188_s1 (human IFN-β), NM_172210.2, NM_172211.2, NM_172212.2, NM_000757.4 (human MCSF), NM_000201.2, Hs00164932_m1, (human ICAM-1), NM_001078.3, NM_001199834.1, NM_080682.2, Hs00365486_m1 (human VCAM-1), NM_000594.2, Hs00174128_m1 (human TNFα), NM_001065.3, Hs00533560_m1 (human TNFR1), NM_001066.2, Hs00153550_m1 (human TNFR2) and M33197 (human GAPDH).

    Techniques: Amplification, Incubation, Expressing, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    Effect of HCV RNA containing cryoprecipitates on the expression of cytokines, chemokines and adhesion molecules. HMEC were stimulated with different concentrations (100×10 6 geq/ml, 200×10 6 geq/ml) of HCV RNA containing cryoprecipitates (HCV) for 12 hours and mRNA expression of selected cytokines and chemokines IL-6 (A), IL-8 (C), IP-10 (E) and adhesion molecule ICAM-1 (G) was analyzed by RT-PCR. Protein synthesis of IL-6 (B), IL-8 (D) and IP-10 (F) was also confirmed by ELISA. Results are given as means ± SD of three experiments done in parallel for each condition and rRNA served as the reference gene. Comparable results were obtained in two series of independent experiments. Statistically significant differences to the control are depicted with * = p≤0.05.

    Journal: PLoS ONE

    Article Title: Hepatitis C Virus Induced Endothelial Inflammatory Response Depends on the Functional Expression of TNFα Receptor Subtype 2

    doi: 10.1371/journal.pone.0113351

    Figure Lengend Snippet: Effect of HCV RNA containing cryoprecipitates on the expression of cytokines, chemokines and adhesion molecules. HMEC were stimulated with different concentrations (100×10 6 geq/ml, 200×10 6 geq/ml) of HCV RNA containing cryoprecipitates (HCV) for 12 hours and mRNA expression of selected cytokines and chemokines IL-6 (A), IL-8 (C), IP-10 (E) and adhesion molecule ICAM-1 (G) was analyzed by RT-PCR. Protein synthesis of IL-6 (B), IL-8 (D) and IP-10 (F) was also confirmed by ELISA. Results are given as means ± SD of three experiments done in parallel for each condition and rRNA served as the reference gene. Comparable results were obtained in two series of independent experiments. Statistically significant differences to the control are depicted with * = p≤0.05.

    Article Snippet: Sequences were used as indicated or pre-developed Taq Man assay reagents or primers and probes were purchased from Applied Biosystems: NM_003265.2, HS00152933_m1 (human TLR3), NM_014314.3, Hs00204833_m1 (human RIG-I), NM_022168.2, Hs0170332_m1 (human MDA5), NM_000600.3, Hs00174131_m1 (human IL-6), NM_000584.2, Hs00174103_m1 (human IL-8), NM_002985.2, Hs00174575_m1 (human RANTES), NM_002982.3, Hs00234140_m1, (human MCP-1), NM_001565.2, Hs00171042_m1 (human IP-10), FP: CCT TCC TCC TGT CTG ATG GA ; RP: ACT GGT TGC CAT CAA ACT CC ; T1: 6FAM CAG ACA TGA CTT TGG ATT TCC CCA GG (human IFN-α), NM_002176.2, Hs00277188_s1 (human IFN-β), NM_172210.2, NM_172211.2, NM_172212.2, NM_000757.4 (human MCSF), NM_000201.2, Hs00164932_m1, (human ICAM-1), NM_001078.3, NM_001199834.1, NM_080682.2, Hs00365486_m1 (human VCAM-1), NM_000594.2, Hs00174128_m1 (human TNFα), NM_001065.3, Hs00533560_m1 (human TNFR1), NM_001066.2, Hs00153550_m1 (human TNFR2) and M33197 (human GAPDH).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    Effect of fullerenol on the relative gene expression levels of adhesion molecules in mouse brain microvascular endothelial cell (MBMEC) cultures under basal and inflammatory conditions. Real time PCR analysis of the expression levels of ICAM-1 ( A ) and VCAM-1 ( B ) in MBMEC after exposure to interferon-γ and tumor necrosis factor-α (inflamed; I + T; 100 IU each) and treatment with fullerenol (F; 1, 10 and 100 µg/mL; n = 4) for 18 h compared to cultures under basal (homeostatic milieu) conditions. GAPDH was used as a housekeeping gene. Ctrl, untreated control; Veh, vehicle treatment.

    Journal: International Journal of Molecular Sciences

    Article Title: Effects of Fullerenols on Mouse Brain Microvascular Endothelial Cells

    doi: 10.3390/ijms18081783

    Figure Lengend Snippet: Effect of fullerenol on the relative gene expression levels of adhesion molecules in mouse brain microvascular endothelial cell (MBMEC) cultures under basal and inflammatory conditions. Real time PCR analysis of the expression levels of ICAM-1 ( A ) and VCAM-1 ( B ) in MBMEC after exposure to interferon-γ and tumor necrosis factor-α (inflamed; I + T; 100 IU each) and treatment with fullerenol (F; 1, 10 and 100 µg/mL; n = 4) for 18 h compared to cultures under basal (homeostatic milieu) conditions. GAPDH was used as a housekeeping gene. Ctrl, untreated control; Veh, vehicle treatment.

    Article Snippet: Relative gene expression levels of occludin (assay ID: Mm 00500912_m1, Applied Biosystems), claudin 3 (assay ID: Mm 00515499_s1, Applied Biosystems), claudin 5 (assay ID: Mm 00727012_s1, Applied Biosystems), ICAM-1 (assay ID: Mm 00516023_m1, Applied Biosystems) and VCAM-1 (assay ID: Mm 01320970_m1, Applied Biosystems) were analyzed with a fluorescent TaqMan technology.

    Techniques: Expressing, Real-time Polymerase Chain Reaction

    Effect of fullerenols on the amount of adhesion molecules in mouse brain microvascular endothelial cell (MBMEC) cultures under basal and inflammatory conditions. Western blot analysis and densitometric quantification (normalized to basal or inflamed untreated control cell cultures) of the amount of VCAM-1 ( A – C ) and ICAM-1 ( D – F ) proteins in MBMECs after exposure to interferon-γ and tumor necrosis factor-α (I + T; 100 IU each) ( C , F ), and treatment with fullerenol (F; 1, 10 and 100 µg/mL; n = 6) for 18 h compared to cultures under basal (homeostatic milieu) conditions ( B , E ). β-Actin was used as loading control. Ctrl, untreated control; Veh, vehicle treatment.

    Journal: International Journal of Molecular Sciences

    Article Title: Effects of Fullerenols on Mouse Brain Microvascular Endothelial Cells

    doi: 10.3390/ijms18081783

    Figure Lengend Snippet: Effect of fullerenols on the amount of adhesion molecules in mouse brain microvascular endothelial cell (MBMEC) cultures under basal and inflammatory conditions. Western blot analysis and densitometric quantification (normalized to basal or inflamed untreated control cell cultures) of the amount of VCAM-1 ( A – C ) and ICAM-1 ( D – F ) proteins in MBMECs after exposure to interferon-γ and tumor necrosis factor-α (I + T; 100 IU each) ( C , F ), and treatment with fullerenol (F; 1, 10 and 100 µg/mL; n = 6) for 18 h compared to cultures under basal (homeostatic milieu) conditions ( B , E ). β-Actin was used as loading control. Ctrl, untreated control; Veh, vehicle treatment.

    Article Snippet: Relative gene expression levels of occludin (assay ID: Mm 00500912_m1, Applied Biosystems), claudin 3 (assay ID: Mm 00515499_s1, Applied Biosystems), claudin 5 (assay ID: Mm 00727012_s1, Applied Biosystems), ICAM-1 (assay ID: Mm 00516023_m1, Applied Biosystems) and VCAM-1 (assay ID: Mm 01320970_m1, Applied Biosystems) were analyzed with a fluorescent TaqMan technology.

    Techniques: Western Blot

    Brefeldin A, but not 1-deoxymannojirimycin, inhibits IL-1α-induced cell-surface ICAM-1 expression. A549 cells were preincubated with various concentrations of 1-deoxymannojirimycin (A) or brefeldin A (B) for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P

    Journal: FEBS Open Bio

    Article Title: Ursolic acid, a natural pentacyclic triterpenoid, inhibits intracellular trafficking of proteins and induces accumulation of intercellular adhesion molecule-1 linked to high-mannose-type glycans in the endoplasmic reticulum

    doi: 10.1016/j.fob.2014.02.009

    Figure Lengend Snippet: Brefeldin A, but not 1-deoxymannojirimycin, inhibits IL-1α-induced cell-surface ICAM-1 expression. A549 cells were preincubated with various concentrations of 1-deoxymannojirimycin (A) or brefeldin A (B) for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P

    Article Snippet: By contrast, the localization of ICAM-1 in the 1-deoxymannojirimycin-treated cells was similar to that in control cells, as ICAM-1 was dispersed over the whole cell and a part of ICAM-1 was co-localized with both GM130 and calnexin ( A and B).

    Techniques: Expressing, Incubation, Enzyme-linked Immunosorbent Assay

    Ursolic acid inhibits IL-1α-induced cell-surface ICAM-1 expression. (A–C) A549 cells (A), MCF-7 cells (B), and HUVEC (C) were preincubated with various concentrations of ursolic acid for 1 h and then incubated with (filled circles) or without (open circles) IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P

    Journal: FEBS Open Bio

    Article Title: Ursolic acid, a natural pentacyclic triterpenoid, inhibits intracellular trafficking of proteins and induces accumulation of intercellular adhesion molecule-1 linked to high-mannose-type glycans in the endoplasmic reticulum

    doi: 10.1016/j.fob.2014.02.009

    Figure Lengend Snippet: Ursolic acid inhibits IL-1α-induced cell-surface ICAM-1 expression. (A–C) A549 cells (A), MCF-7 cells (B), and HUVEC (C) were preincubated with various concentrations of ursolic acid for 1 h and then incubated with (filled circles) or without (open circles) IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P

    Article Snippet: By contrast, the localization of ICAM-1 in the 1-deoxymannojirimycin-treated cells was similar to that in control cells, as ICAM-1 was dispersed over the whole cell and a part of ICAM-1 was co-localized with both GM130 and calnexin ( A and B).

    Techniques: Expressing, Incubation, Enzyme-linked Immunosorbent Assay

    Ursolic acid affects N-linked oligosaccharide processing of ICAM-1. (A) A549 cells were treated with various concentrations of tunicamycin for 1 h and then incubated with (+) or without (−) IL-1α (0.25 ng/ml) for 6 h. Cell lysates were analyzed by Western blotting. Data are representative of three independent experiments. (B) A549 cells were preincubated with various concentrations of tunicamycin for 1 h and then incubated with (filled circles) or without (open circles) IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P

    Journal: FEBS Open Bio

    Article Title: Ursolic acid, a natural pentacyclic triterpenoid, inhibits intracellular trafficking of proteins and induces accumulation of intercellular adhesion molecule-1 linked to high-mannose-type glycans in the endoplasmic reticulum

    doi: 10.1016/j.fob.2014.02.009

    Figure Lengend Snippet: Ursolic acid affects N-linked oligosaccharide processing of ICAM-1. (A) A549 cells were treated with various concentrations of tunicamycin for 1 h and then incubated with (+) or without (−) IL-1α (0.25 ng/ml) for 6 h. Cell lysates were analyzed by Western blotting. Data are representative of three independent experiments. (B) A549 cells were preincubated with various concentrations of tunicamycin for 1 h and then incubated with (filled circles) or without (open circles) IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P

    Article Snippet: By contrast, the localization of ICAM-1 in the 1-deoxymannojirimycin-treated cells was similar to that in control cells, as ICAM-1 was dispersed over the whole cell and a part of ICAM-1 was co-localized with both GM130 and calnexin ( A and B).

    Techniques: Incubation, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

    Ursolic acid does not inhibit IL-1α-induced expression of ICAM-1 at the protein level but affects its post-translational modification. A549 cells (A), MCF-7 cells (B), and HUVEC (C) were preincubated with various concentrations of ursolic acid for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h. Cell lysates were analyzed by Western blotting. Data are representative of at least three independent experiments for A549 cells and MCF-7 cells and two independent experiments for HUVEC.

    Journal: FEBS Open Bio

    Article Title: Ursolic acid, a natural pentacyclic triterpenoid, inhibits intracellular trafficking of proteins and induces accumulation of intercellular adhesion molecule-1 linked to high-mannose-type glycans in the endoplasmic reticulum

    doi: 10.1016/j.fob.2014.02.009

    Figure Lengend Snippet: Ursolic acid does not inhibit IL-1α-induced expression of ICAM-1 at the protein level but affects its post-translational modification. A549 cells (A), MCF-7 cells (B), and HUVEC (C) were preincubated with various concentrations of ursolic acid for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h. Cell lysates were analyzed by Western blotting. Data are representative of at least three independent experiments for A549 cells and MCF-7 cells and two independent experiments for HUVEC.

    Article Snippet: By contrast, the localization of ICAM-1 in the 1-deoxymannojirimycin-treated cells was similar to that in control cells, as ICAM-1 was dispersed over the whole cell and a part of ICAM-1 was co-localized with both GM130 and calnexin ( A and B).

    Techniques: Expressing, Modification, Incubation, Western Blot

    Ursolic acid induces accumulation of ICAM-1 in ER. A549 cells were preincubated with or without ursolic acid (50 μM) for 1 h and then incubated with or without IL-1α (0.25 ng/ml) for 6 h in the presence or absence of ursolic acid. Cells were fixed and stained for ICAM-1 (green), together with GM130 (red) (A) and calnexin (red) (B) as markers of Golgi apparatus and ER, respectively. Panels A and B show higher magnification images of representative cells in Figs. S3 and S4 , respectively. Scale bars represent 20 μm. Data are representative of at least three independent experiments. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: FEBS Open Bio

    Article Title: Ursolic acid, a natural pentacyclic triterpenoid, inhibits intracellular trafficking of proteins and induces accumulation of intercellular adhesion molecule-1 linked to high-mannose-type glycans in the endoplasmic reticulum

    doi: 10.1016/j.fob.2014.02.009

    Figure Lengend Snippet: Ursolic acid induces accumulation of ICAM-1 in ER. A549 cells were preincubated with or without ursolic acid (50 μM) for 1 h and then incubated with or without IL-1α (0.25 ng/ml) for 6 h in the presence or absence of ursolic acid. Cells were fixed and stained for ICAM-1 (green), together with GM130 (red) (A) and calnexin (red) (B) as markers of Golgi apparatus and ER, respectively. Panels A and B show higher magnification images of representative cells in Figs. S3 and S4 , respectively. Scale bars represent 20 μm. Data are representative of at least three independent experiments. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: By contrast, the localization of ICAM-1 in the 1-deoxymannojirimycin-treated cells was similar to that in control cells, as ICAM-1 was dispersed over the whole cell and a part of ICAM-1 was co-localized with both GM130 and calnexin ( A and B).

    Techniques: Incubation, Staining

    Ursolic acid inhibits intracellular protein transport from ER to Golgi apparatus in a manner distinct from brefeldin A. A549 cells were preincubated with or without ursolic acid (50 μM), brefeldin A (100 nM) or 1-deoxymannojirimycin (100 μM) for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h in the presence or absence of the compounds. Cells were fixed and stained for ICAM-1 (green), together with GM130 (red) (A) and calnexin (red) (B) as markers of Golgi apparatus and ER, respectively. Panels A and B show higher magnification images of representative cells in Figs. S5 and S6 , respectively. Scale bars represent 20 μm. Data are representative of at least three independent experiments. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: FEBS Open Bio

    Article Title: Ursolic acid, a natural pentacyclic triterpenoid, inhibits intracellular trafficking of proteins and induces accumulation of intercellular adhesion molecule-1 linked to high-mannose-type glycans in the endoplasmic reticulum

    doi: 10.1016/j.fob.2014.02.009

    Figure Lengend Snippet: Ursolic acid inhibits intracellular protein transport from ER to Golgi apparatus in a manner distinct from brefeldin A. A549 cells were preincubated with or without ursolic acid (50 μM), brefeldin A (100 nM) or 1-deoxymannojirimycin (100 μM) for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h in the presence or absence of the compounds. Cells were fixed and stained for ICAM-1 (green), together with GM130 (red) (A) and calnexin (red) (B) as markers of Golgi apparatus and ER, respectively. Panels A and B show higher magnification images of representative cells in Figs. S5 and S6 , respectively. Scale bars represent 20 μm. Data are representative of at least three independent experiments. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: By contrast, the localization of ICAM-1 in the 1-deoxymannojirimycin-treated cells was similar to that in control cells, as ICAM-1 was dispersed over the whole cell and a part of ICAM-1 was co-localized with both GM130 and calnexin ( A and B).

    Techniques: Incubation, Staining

    Expression of pCICAM-1 and pCLFA-3 on human rhabdomyosarcoma ( RD ) cells in vitro . RD cells were transfected with pCDNA3 (control), pCICAM-1, or pCLFA-3. Three days after transfection, the cells were removed from the plates and were analyzed by FACS ® analysis using either control antibodies, α–intracellular adhesion molecule-1 ( ICAM-1 ), or α–lymphocyte function associated-3 ( LFA-3 ) antibodies to detect expression of the transfected gene product.

    Journal: Journal of Clinical Investigation

    Article Title: Intracellular adhesion molecule-1 modulates ?-chemokines and directly costimulates T cells in vivo

    doi:

    Figure Lengend Snippet: Expression of pCICAM-1 and pCLFA-3 on human rhabdomyosarcoma ( RD ) cells in vitro . RD cells were transfected with pCDNA3 (control), pCICAM-1, or pCLFA-3. Three days after transfection, the cells were removed from the plates and were analyzed by FACS ® analysis using either control antibodies, α–intracellular adhesion molecule-1 ( ICAM-1 ), or α–lymphocyte function associated-3 ( LFA-3 ) antibodies to detect expression of the transfected gene product.

    Article Snippet: The effects of ICAM-1 and LFA-3 could be dependent on B7-CD28 signals, or they could represent an alternative synergistic pathway for driving CTL induction in vivo .

    Techniques: Expressing, In Vitro, Transfection, FACS

    ICAM-1 expression in aorta after 12 weeks. A: Immunohistochemistry analyses of ICAM-1 in aorta (The arrows indicate positive expressions). B: Mean optical density values of ICAM-1. The optical density of ICAM-1 were quantitatively analyzed with Image - Pro Plus after 12 weeks. C: control, standard diet for 12 weeks ( n = 5); H: high-cholesterol diet for 12 weeks ( n = 5); HO: high-cholesterol diet with ogi for 12 weeks ( n = 5); HOH: high-cholesterol diet with ogi and hesperidin for 12 weeks ( n = 5); HOG: high-cholesterol diet with ogi and ginger for 12 weeks ( n = 5); HE: high-cholesterol diet with ezetimibe for 12 weeks ( n = 5). * P

    Journal: Yonago Acta Medica

    Article Title: Components of Boiogito Suppress the Progression of Hypercholesterolemia and Fatty Liver Induced by High-Cholesterol Diet in Rats

    doi:

    Figure Lengend Snippet: ICAM-1 expression in aorta after 12 weeks. A: Immunohistochemistry analyses of ICAM-1 in aorta (The arrows indicate positive expressions). B: Mean optical density values of ICAM-1. The optical density of ICAM-1 were quantitatively analyzed with Image - Pro Plus after 12 weeks. C: control, standard diet for 12 weeks ( n = 5); H: high-cholesterol diet for 12 weeks ( n = 5); HO: high-cholesterol diet with ogi for 12 weeks ( n = 5); HOH: high-cholesterol diet with ogi and hesperidin for 12 weeks ( n = 5); HOG: high-cholesterol diet with ogi and ginger for 12 weeks ( n = 5); HE: high-cholesterol diet with ezetimibe for 12 weeks ( n = 5). * P

    Article Snippet: Anti-ICAM-1 (Abcam, Cambridge, United Kingdom) was used.

    Techniques: Expressing, Immunohistochemistry

    ICAM-1 and RBP4 concentrations in serum. ICAM-1 and RBP4 concentrations in standard diet group (C, n = 5), high-cholesterol diet group (H, n = 5), high-cholesterol diet with ogi group (HO, n = 5), high-cholesterol diet with ogi and hesperidin group (HOH, n = 5), high-cholesterol diet with ogi and ginger group (HOG, n = 5) and high-cholesterol diet with ezetimibe group (HE, n = 5). Dotted and shaded columns represent 6 and 12 weeks, respectively. * P

    Journal: Yonago Acta Medica

    Article Title: Components of Boiogito Suppress the Progression of Hypercholesterolemia and Fatty Liver Induced by High-Cholesterol Diet in Rats

    doi:

    Figure Lengend Snippet: ICAM-1 and RBP4 concentrations in serum. ICAM-1 and RBP4 concentrations in standard diet group (C, n = 5), high-cholesterol diet group (H, n = 5), high-cholesterol diet with ogi group (HO, n = 5), high-cholesterol diet with ogi and hesperidin group (HOH, n = 5), high-cholesterol diet with ogi and ginger group (HOG, n = 5) and high-cholesterol diet with ezetimibe group (HE, n = 5). Dotted and shaded columns represent 6 and 12 weeks, respectively. * P

    Article Snippet: Anti-ICAM-1 (Abcam, Cambridge, United Kingdom) was used.

    Techniques:

    Graphics and histograms (cytoflow data) of the effect of MMF (50, 100, 150, 200, 250, and 300 μg/mL) on TNF-α-induced expression of ICAM-1 in HCAECs (A, B) and HCMSMCs (C, D) after 18 h. Negative control (dotted line) and ICAM-1 expression in untreated cells (grey line) are included.

    Journal: BMC Cardiovascular Disorders

    Article Title: Effects of mycophenolate mofetil on key pattern of coronary restenosis: a cascade of in vitro and ex vivo models

    doi: 10.1186/1471-2261-5-9

    Figure Lengend Snippet: Graphics and histograms (cytoflow data) of the effect of MMF (50, 100, 150, 200, 250, and 300 μg/mL) on TNF-α-induced expression of ICAM-1 in HCAECs (A, B) and HCMSMCs (C, D) after 18 h. Negative control (dotted line) and ICAM-1 expression in untreated cells (grey line) are included.

    Article Snippet: Effect of MMF on ICAM-1: Flow cytometry studies The effects of MMF (50, 100, 150, 200, 250, and 300 μg/mL) on the TNF-α induced expression of ICAM-1 are demonstrated in Figure .

    Techniques: Expressing, Negative Control

    Northern blots and relative band densities of TNF-α-induced expression of ICAM-1 mRNA after incubation of HCAECs and HCMSMCs with 50, 100, 150, 200, 250, and 300 μg/mL of MMF.

    Journal: BMC Cardiovascular Disorders

    Article Title: Effects of mycophenolate mofetil on key pattern of coronary restenosis: a cascade of in vitro and ex vivo models

    doi: 10.1186/1471-2261-5-9

    Figure Lengend Snippet: Northern blots and relative band densities of TNF-α-induced expression of ICAM-1 mRNA after incubation of HCAECs and HCMSMCs with 50, 100, 150, 200, 250, and 300 μg/mL of MMF.

    Article Snippet: Effect of MMF on ICAM-1: Flow cytometry studies The effects of MMF (50, 100, 150, 200, 250, and 300 μg/mL) on the TNF-α induced expression of ICAM-1 are demonstrated in Figure .

    Techniques: Northern Blot, Expressing, Incubation

    TCR-mediated absorption of membrane vesicles. ( a ) Absorption of B7-1 by purified naïve or activated CD8 + 2C cells after incubation for 1 h with L d .B7-1 or L d .B7-1.ICAM-1 Dros APCs loaded with QL9 peptide at 10 μM; activated T cells were prepared by preculturing cells for 12 h with PMA plus ionomycin. T cells and APCs were either cultured together (intact APCs) or separated from each other by placing APCs in a transwell (pore size 3 μm); Dros cells are large ( > 20 μm) and were unable to pass through the Transwell membrane. After culture, T cells were stained for B7-1, L d , and CD8 and then examined by flow cytometry. The data show staining of gated CD8 + cells. ( a Upper ) B7-1 staining of resting vs. activated 2C cells after culture with L d .B7-1 vs. L d .B7-1.ICAM-1 Dros APCs. ( a Lower ) B7-1 and L d staining of activated 2C cells cultured with L d .B7-1.ICAM-1 Dros APCs in the absence or presence of anti-LFA-1 mAb (5 ng/ml). ( b ) Morphology of membrane vesicles. Culture supernatants from L d .B7-1.ICAM-1 Dros APCs were depleted of cell debris, then ultracentrifuged. ( Left ) Electron microscopic view of pelleted material is shown at low ( Upper ) and high ( Lower ) magnification. (Bar, 200 nm.) Much of the material in the pellet shows the morphology of membrane vesicles; cell debris, more prominent in other fields, is also present. ( Right ) Electron microscopic view of magnetic beads that were coated with anti-ICAM-1 mAb ( Lower ) or an Ig isotype-matched control mAb ( Upper ) before incubation with the above membrane vesicles.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Direct stimulation of na?ve T cells by membrane vesicles from antigen-presenting cells: Distinct roles for CD54 and B7 molecules

    doi: 10.1073/pnas.1131852100

    Figure Lengend Snippet: TCR-mediated absorption of membrane vesicles. ( a ) Absorption of B7-1 by purified naïve or activated CD8 + 2C cells after incubation for 1 h with L d .B7-1 or L d .B7-1.ICAM-1 Dros APCs loaded with QL9 peptide at 10 μM; activated T cells were prepared by preculturing cells for 12 h with PMA plus ionomycin. T cells and APCs were either cultured together (intact APCs) or separated from each other by placing APCs in a transwell (pore size 3 μm); Dros cells are large ( > 20 μm) and were unable to pass through the Transwell membrane. After culture, T cells were stained for B7-1, L d , and CD8 and then examined by flow cytometry. The data show staining of gated CD8 + cells. ( a Upper ) B7-1 staining of resting vs. activated 2C cells after culture with L d .B7-1 vs. L d .B7-1.ICAM-1 Dros APCs. ( a Lower ) B7-1 and L d staining of activated 2C cells cultured with L d .B7-1.ICAM-1 Dros APCs in the absence or presence of anti-LFA-1 mAb (5 ng/ml). ( b ) Morphology of membrane vesicles. Culture supernatants from L d .B7-1.ICAM-1 Dros APCs were depleted of cell debris, then ultracentrifuged. ( Left ) Electron microscopic view of pelleted material is shown at low ( Upper ) and high ( Lower ) magnification. (Bar, 200 nm.) Much of the material in the pellet shows the morphology of membrane vesicles; cell debris, more prominent in other fields, is also present. ( Right ) Electron microscopic view of magnetic beads that were coated with anti-ICAM-1 mAb ( Lower ) or an Ig isotype-matched control mAb ( Upper ) before incubation with the above membrane vesicles.

    Article Snippet: Anti-ICAM-1 (YN1/1.7.4) was purchased from e-Bioscience (San Diego).

    Techniques: Purification, Incubation, Cell Culture, Staining, Flow Cytometry, Cytometry, Magnetic Beads

    Accessory molecules required for proliferative responses of naïve 2C cells to peptide-loaded membrane vesicles. ( a ) Purified resting normal (CD28 + ) 2C CD8 + T cells (5 × 10 4 per well) were cultured with membrane vesicles (100 μg/ml, 10 μg per well) purified from L d .B7-1, L d .ICAM-1, and L d .B7-1.ICAM-1 Dros APCs loaded with 10 μM QL9 peptide in a 96-well plate. The cultures were pulsed with 3 HTdR after 40 h, and 3 HTdR incorporation was measured after 48 h. The data show mean cpm values for triplicate cultures; SDs were very small and are not shown. ( b ) Purified normal 2C or 2C.CD28 – / – CD8 + T cells were cultured with QL9-loaded L d .B7-1.ICAM-1 membrane vesicles as described in a . For mAb blocking, 2C T cells were preincubated with 5 μg/ml anti-LFA-1 mAb or anti-CD45 mAb (as an isotype control mAb) for 30 min on ice before culture, and the mAbs were left in the cultures during incubation at 37°C. For size fractionation of resuspended vesicles after ultracentrifugation, solutions of membrane vesicles were filtered by using syringe filters with the pore sizes indicated. After filtration, protein concentrations in the filtrates were measured and, after loading with QL9 peptide (10 μM), the vesicles were added to the cultures at 10 μg per well. As in a , the data show mean levels of 3 HTdR incorporation (cpm) for triplicate cultures. ( c ) Purified resting 2C T cells (5 × 10 4 per well) were cultured with intact L d .B7-1.ICAM-1 Dros APCs (loaded with 0.01 μM QL9; see Materials and Methods ) or with purified L d .B7-1.ICAM-1 membrane vesicles (loaded with 10 μM QL9) at 100 μg/ml. The cultures were pulsed with 3 HTdR for 8 h before harvest. The data show 3 HTdR incorporation (mean cpm of triplicate cultures) on days 1–4 of culture. ( d ) CFSE-labeled purified resting normal 2C CD8 + T cells were cultured with L d .B7-1.ICAM-1 membrane vesicles as described in a for 15 or 63 h and then stained with CD8 mAb. Histograms show CFSE staining on gated CD8 + T cells. The data are representative of several experiments. ( e ) PMA-treated or untreated purified 2C T cells (5 × 10 4 per well) were cultured with various concentrations of membrane vesicles (L d .B7-1.ICAM-1) loaded with 10 μM QL9 peptide for 48 h. For PMA treatment, resting 2C T cells were incubated with PMA (50 ng/ml) for 30 min at 37°C and then washed thoroughly; as in b , suspensions of membrane vesicles were filtered by using syringe filters with the indicated pore sizes before addition to 2C cells. As in a , the data show mean cpm values for 3 HTdR incorporation on day 2 of culture. ( f ) Resting purified normal 2C T cells were cultured as in a with 100 μg/ml L d .B7-1.ICAM-1 membrane vesicles; vesicles were loaded with QL9 or p2Ca peptide at the concentrations shown. 3 HTdR incorporation was measured on day 2.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Direct stimulation of na?ve T cells by membrane vesicles from antigen-presenting cells: Distinct roles for CD54 and B7 molecules

    doi: 10.1073/pnas.1131852100

    Figure Lengend Snippet: Accessory molecules required for proliferative responses of naïve 2C cells to peptide-loaded membrane vesicles. ( a ) Purified resting normal (CD28 + ) 2C CD8 + T cells (5 × 10 4 per well) were cultured with membrane vesicles (100 μg/ml, 10 μg per well) purified from L d .B7-1, L d .ICAM-1, and L d .B7-1.ICAM-1 Dros APCs loaded with 10 μM QL9 peptide in a 96-well plate. The cultures were pulsed with 3 HTdR after 40 h, and 3 HTdR incorporation was measured after 48 h. The data show mean cpm values for triplicate cultures; SDs were very small and are not shown. ( b ) Purified normal 2C or 2C.CD28 – / – CD8 + T cells were cultured with QL9-loaded L d .B7-1.ICAM-1 membrane vesicles as described in a . For mAb blocking, 2C T cells were preincubated with 5 μg/ml anti-LFA-1 mAb or anti-CD45 mAb (as an isotype control mAb) for 30 min on ice before culture, and the mAbs were left in the cultures during incubation at 37°C. For size fractionation of resuspended vesicles after ultracentrifugation, solutions of membrane vesicles were filtered by using syringe filters with the pore sizes indicated. After filtration, protein concentrations in the filtrates were measured and, after loading with QL9 peptide (10 μM), the vesicles were added to the cultures at 10 μg per well. As in a , the data show mean levels of 3 HTdR incorporation (cpm) for triplicate cultures. ( c ) Purified resting 2C T cells (5 × 10 4 per well) were cultured with intact L d .B7-1.ICAM-1 Dros APCs (loaded with 0.01 μM QL9; see Materials and Methods ) or with purified L d .B7-1.ICAM-1 membrane vesicles (loaded with 10 μM QL9) at 100 μg/ml. The cultures were pulsed with 3 HTdR for 8 h before harvest. The data show 3 HTdR incorporation (mean cpm of triplicate cultures) on days 1–4 of culture. ( d ) CFSE-labeled purified resting normal 2C CD8 + T cells were cultured with L d .B7-1.ICAM-1 membrane vesicles as described in a for 15 or 63 h and then stained with CD8 mAb. Histograms show CFSE staining on gated CD8 + T cells. The data are representative of several experiments. ( e ) PMA-treated or untreated purified 2C T cells (5 × 10 4 per well) were cultured with various concentrations of membrane vesicles (L d .B7-1.ICAM-1) loaded with 10 μM QL9 peptide for 48 h. For PMA treatment, resting 2C T cells were incubated with PMA (50 ng/ml) for 30 min at 37°C and then washed thoroughly; as in b , suspensions of membrane vesicles were filtered by using syringe filters with the indicated pore sizes before addition to 2C cells. As in a , the data show mean cpm values for 3 HTdR incorporation on day 2 of culture. ( f ) Resting purified normal 2C T cells were cultured as in a with 100 μg/ml L d .B7-1.ICAM-1 membrane vesicles; vesicles were loaded with QL9 or p2Ca peptide at the concentrations shown. 3 HTdR incorporation was measured on day 2.

    Article Snippet: Anti-ICAM-1 (YN1/1.7.4) was purchased from e-Bioscience (San Diego).

    Techniques: Purification, Cell Culture, Blocking Assay, Incubation, Fractionation, Filtration, Labeling, Staining

    TCR-mediated absorption of membrane vesicles requires LFA-1/ICAM-1 interaction. ( a ) Absorption of QL9-loaded L d .B7-1.ICAM-1 Dros APCs membrane vesicles by resting B6 and 2C.CD28 — / — CD8 + cells. T cells were incubated for 45 min with 200 μg/ml L d .B7-1.ICAM-1 membrane vesicles that had been loaded with 10 μM QL9 peptide; control cells were incubated in the absence of vesicles. The T cells were then washed, stained for B7-1, L d , and CD8, and examined by flow cytometry. The data show representative staining for B7-1 and L d on gated CD8 + cells. ( b ) 2C cell absorption of vesicles derived from L d .B7-1.ICAM-1, L d .B7-1, and L d .ICAM-1 Dros APCs. 2C cells on a normal (not a CD28 — / — ) background were incubated with membrane vesicles and then stained as for a ; vesicles were loaded either with QL9 or control PIA peptide at 10 μM. The data show representative staining for L d on gated CD8 + cells after incubation with vesicles derived from the indicated Dros cells.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Direct stimulation of na?ve T cells by membrane vesicles from antigen-presenting cells: Distinct roles for CD54 and B7 molecules

    doi: 10.1073/pnas.1131852100

    Figure Lengend Snippet: TCR-mediated absorption of membrane vesicles requires LFA-1/ICAM-1 interaction. ( a ) Absorption of QL9-loaded L d .B7-1.ICAM-1 Dros APCs membrane vesicles by resting B6 and 2C.CD28 — / — CD8 + cells. T cells were incubated for 45 min with 200 μg/ml L d .B7-1.ICAM-1 membrane vesicles that had been loaded with 10 μM QL9 peptide; control cells were incubated in the absence of vesicles. The T cells were then washed, stained for B7-1, L d , and CD8, and examined by flow cytometry. The data show representative staining for B7-1 and L d on gated CD8 + cells. ( b ) 2C cell absorption of vesicles derived from L d .B7-1.ICAM-1, L d .B7-1, and L d .ICAM-1 Dros APCs. 2C cells on a normal (not a CD28 — / — ) background were incubated with membrane vesicles and then stained as for a ; vesicles were loaded either with QL9 or control PIA peptide at 10 μM. The data show representative staining for L d on gated CD8 + cells after incubation with vesicles derived from the indicated Dros cells.

    Article Snippet: Anti-ICAM-1 (YN1/1.7.4) was purchased from e-Bioscience (San Diego).

    Techniques: Incubation, Staining, Flow Cytometry, Cytometry, Derivative Assay

    Effector functions of 2C CD8 + cells stimulated with Dros APC membrane vesicles. As for proliferation, 2C CD8 + cells at 5 × 10 4 cells per well were stimulated with 100 μg/ml L d .B7-1.ICAM-1 membrane vesicles loaded with QL9 or p2Ca peptides at the concentrations shown. Concentrations of IFN-γ ( a ) and IL-2 ( b ) in culture supernatants collected at 24–60 h are shown; cytokines were measured by ELISA. The data represents means (±SD) of triplicate cultures. ( c ) CTL activity of 2C cells cultured with vesicles as above for 60 h. The data show mean percent of lysis (±SD) of P815 (L d ) target cells for triplicate cultures; lysis was measured over 4 h. In some cultures, the activated 2C cells were preincubated with 1B2 anti-clonotypic mAb (10 μg/ml). Note that P815 cells were not supplemented with exogenous peptide.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Direct stimulation of na?ve T cells by membrane vesicles from antigen-presenting cells: Distinct roles for CD54 and B7 molecules

    doi: 10.1073/pnas.1131852100

    Figure Lengend Snippet: Effector functions of 2C CD8 + cells stimulated with Dros APC membrane vesicles. As for proliferation, 2C CD8 + cells at 5 × 10 4 cells per well were stimulated with 100 μg/ml L d .B7-1.ICAM-1 membrane vesicles loaded with QL9 or p2Ca peptides at the concentrations shown. Concentrations of IFN-γ ( a ) and IL-2 ( b ) in culture supernatants collected at 24–60 h are shown; cytokines were measured by ELISA. The data represents means (±SD) of triplicate cultures. ( c ) CTL activity of 2C cells cultured with vesicles as above for 60 h. The data show mean percent of lysis (±SD) of P815 (L d ) target cells for triplicate cultures; lysis was measured over 4 h. In some cultures, the activated 2C cells were preincubated with 1B2 anti-clonotypic mAb (10 μg/ml). Note that P815 cells were not supplemented with exogenous peptide.

    Article Snippet: Anti-ICAM-1 (YN1/1.7.4) was purchased from e-Bioscience (San Diego).

    Techniques: Enzyme-linked Immunosorbent Assay, CTL Assay, Activity Assay, Cell Culture, Lysis

    Pearson's correlation analysis between the mean value of ICAM-1 and NF-κB expression in the 4 treatment groups. ICAM, intercellular adhesion molecule; NF, nuclear factor.

    Journal: Molecular Medicine Reports

    Article Title: Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression

    doi: 10.3892/mmr.2017.7205

    Figure Lengend Snippet: Pearson's correlation analysis between the mean value of ICAM-1 and NF-κB expression in the 4 treatment groups. ICAM, intercellular adhesion molecule; NF, nuclear factor.

    Article Snippet: Followed by incubation with anti-ICAM-1 (mouse monoclonal antibody, cat. no. 554967; 1:50 dilution; BD Pharmingen; BD Biosciences, Franklin Lakes, NJ, USA), MMP-9 (mouse monoclonal antibody, cat. no. ab58803; 1:700 dilution; Abcam, Cambridge, UK), caspase-3 (rabbit polyclonal antibody, cat. no. 9662s; 1:700 dilution; Cell Signaling Technology, Inc., Danvers, MA, USA), and NF-κB-p65 (mouse monoclonal antibody, cat. no. 8242s; 1:800 dilution; Cell Signaling Technology, Inc.) antibodies at 4°C overnight.

    Techniques: Expressing

    Effect of curcumin on ICAM-1 expression in the whole cortex, penumbra and core area as detected by immunohistochemistry. (A) Positive staining was visualized in brown color and indicated by white arrows. Scale bar, 100 µm. (B) Quantification of ICAM-1 expression. **P≤0.01, with comparisons indicated by brackets. ICAM, intercellular adhesion molecule; MCAO, middle cerebral artery occlusion; CUR, curcumin; CORN, corn oil (vehicle control); IOD, integrated optical density.

    Journal: Molecular Medicine Reports

    Article Title: Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression

    doi: 10.3892/mmr.2017.7205

    Figure Lengend Snippet: Effect of curcumin on ICAM-1 expression in the whole cortex, penumbra and core area as detected by immunohistochemistry. (A) Positive staining was visualized in brown color and indicated by white arrows. Scale bar, 100 µm. (B) Quantification of ICAM-1 expression. **P≤0.01, with comparisons indicated by brackets. ICAM, intercellular adhesion molecule; MCAO, middle cerebral artery occlusion; CUR, curcumin; CORN, corn oil (vehicle control); IOD, integrated optical density.

    Article Snippet: Followed by incubation with anti-ICAM-1 (mouse monoclonal antibody, cat. no. 554967; 1:50 dilution; BD Pharmingen; BD Biosciences, Franklin Lakes, NJ, USA), MMP-9 (mouse monoclonal antibody, cat. no. ab58803; 1:700 dilution; Abcam, Cambridge, UK), caspase-3 (rabbit polyclonal antibody, cat. no. 9662s; 1:700 dilution; Cell Signaling Technology, Inc., Danvers, MA, USA), and NF-κB-p65 (mouse monoclonal antibody, cat. no. 8242s; 1:800 dilution; Cell Signaling Technology, Inc.) antibodies at 4°C overnight.

    Techniques: Expressing, Immunohistochemistry, Staining

    AS-IV decreased the serum levels of TNF- α , MCP-1, and ICAM-1 in rats with ischemic AKI. Serum levels of TNF- α (a), MCP-1 (b), and ICAM-1 (c) in sham, vehicle-, or AS-IV-pretreated rats at 12 h of reperfusion. Serum levels of TNF- α (d), MCP-1 (e), and ICAM-1 (f) in sham, vehicle-, or AS-IV-pretreated rats at 24 h of reperfusion. Results are expressed as mean ± SD ( n = 8). * P

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Preventive Effects of a Natural Anti-Inflammatory Agent, Astragaloside IV, on Ischemic Acute Kidney Injury in Rats

    doi: 10.1155/2013/284025

    Figure Lengend Snippet: AS-IV decreased the serum levels of TNF- α , MCP-1, and ICAM-1 in rats with ischemic AKI. Serum levels of TNF- α (a), MCP-1 (b), and ICAM-1 (c) in sham, vehicle-, or AS-IV-pretreated rats at 12 h of reperfusion. Serum levels of TNF- α (d), MCP-1 (e), and ICAM-1 (f) in sham, vehicle-, or AS-IV-pretreated rats at 24 h of reperfusion. Results are expressed as mean ± SD ( n = 8). * P

    Article Snippet: AS-IV Decreased the Serum Levels of MCP-1, ICAM-1, and TNF-α in Rats with Ischemic AKI Compared with the corresponding sham-operated rats, there was a significant increase in serum levels of MCP-1, ICAM-1, and TNF-α at 12 h of reperfusion in rats with ischemic AKI.

    Techniques:

    AS-IV downregulated the mRNA expression of TNF- α , MCP-1, and ICAM-1 in rats with ischemic AKI. Representative real-time PCR of TNF- α (a), MCP-1 (b), and ICAM-1 (c) in renal tissues from sham, vehicle-, or AS-IV-pretreated rats at 12 h of reperfusion. Representative real-time PCR of TNF- α (d), MCP-1 (e), and ICAM-1 (f) in renal tissues from sham, vehicle-, or AS-IV-pretreated rats at 24 h of reperfusion. Results are expressed as mean ± SD. * P

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Preventive Effects of a Natural Anti-Inflammatory Agent, Astragaloside IV, on Ischemic Acute Kidney Injury in Rats

    doi: 10.1155/2013/284025

    Figure Lengend Snippet: AS-IV downregulated the mRNA expression of TNF- α , MCP-1, and ICAM-1 in rats with ischemic AKI. Representative real-time PCR of TNF- α (a), MCP-1 (b), and ICAM-1 (c) in renal tissues from sham, vehicle-, or AS-IV-pretreated rats at 12 h of reperfusion. Representative real-time PCR of TNF- α (d), MCP-1 (e), and ICAM-1 (f) in renal tissues from sham, vehicle-, or AS-IV-pretreated rats at 24 h of reperfusion. Results are expressed as mean ± SD. * P

    Article Snippet: AS-IV Decreased the Serum Levels of MCP-1, ICAM-1, and TNF-α in Rats with Ischemic AKI Compared with the corresponding sham-operated rats, there was a significant increase in serum levels of MCP-1, ICAM-1, and TNF-α at 12 h of reperfusion in rats with ischemic AKI.

    Techniques: Expressing, Real-time Polymerase Chain Reaction

    AS-IV reduced the protein content of MCP-1, ICAM-1, and TNF- α in rats with ischemic AKI. The protein content of TNF- α (a), MCP-1 (b), and ICAM-1 (c) in renal tissues from sham, vehicle-, or AS-IV-pretreated rats at 12 h of reperfusion. The protein content of TNF- α (d), MCP-1 (e), and ICAM-1 (f) in renal tissues from sham, vehicle-, or AS-IV-pretreated rats at 24 h of reperfusion. Results are expressed as mean ± SD ( n = 8). * P

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Preventive Effects of a Natural Anti-Inflammatory Agent, Astragaloside IV, on Ischemic Acute Kidney Injury in Rats

    doi: 10.1155/2013/284025

    Figure Lengend Snippet: AS-IV reduced the protein content of MCP-1, ICAM-1, and TNF- α in rats with ischemic AKI. The protein content of TNF- α (a), MCP-1 (b), and ICAM-1 (c) in renal tissues from sham, vehicle-, or AS-IV-pretreated rats at 12 h of reperfusion. The protein content of TNF- α (d), MCP-1 (e), and ICAM-1 (f) in renal tissues from sham, vehicle-, or AS-IV-pretreated rats at 24 h of reperfusion. Results are expressed as mean ± SD ( n = 8). * P

    Article Snippet: AS-IV Decreased the Serum Levels of MCP-1, ICAM-1, and TNF-α in Rats with Ischemic AKI Compared with the corresponding sham-operated rats, there was a significant increase in serum levels of MCP-1, ICAM-1, and TNF-α at 12 h of reperfusion in rats with ischemic AKI.

    Techniques:

    Adhesion of (a) CS2 IE and (b) CS2KO9 IE to immobilized receptors, expressed as IE bound/mm 2 . Data shown are the mean + SEM of two or more independent experiments, performed in triplicate. CSA, chondroitin sulphate A; CSA+10 μg/ml, Adhesion to CSA in presence of free CSA at 10 μg/ml; HCSPG, human chondroitin sulphate proteoglycan; ICAM-1, intercellular adhesion molecule 1. HA, hyaluronic acid; FG, fibrinogen.

    Journal: Malaria Journal

    Article Title: Characterization of VAR2CSA-deficient Plasmodium falciparum-infected erythrocytes selected for adhesion to the BeWo placental cell line

    doi: 10.1186/1475-2875-7-51

    Figure Lengend Snippet: Adhesion of (a) CS2 IE and (b) CS2KO9 IE to immobilized receptors, expressed as IE bound/mm 2 . Data shown are the mean + SEM of two or more independent experiments, performed in triplicate. CSA, chondroitin sulphate A; CSA+10 μg/ml, Adhesion to CSA in presence of free CSA at 10 μg/ml; HCSPG, human chondroitin sulphate proteoglycan; ICAM-1, intercellular adhesion molecule 1. HA, hyaluronic acid; FG, fibrinogen.

    Article Snippet: To determine whether CS2KO9 IE which adhered to immobilized ICAM-1 also adhered to ICAM-1 on BeWo cells or placental sections, a blocking antibody to ICAM-1 was used.

    Techniques:

    Adhesion to human placental tissue cryosections. Adhesion levels of IE in the intervillous space (IVS), to syncytiotrophoblast (SCT) and over the villus (V) is shown compared to untreated (control) sections present on each slide. (a) Adhesion of CS2 (white bars) and CS2KO9 (black bars) IE in the presence of CSA (100 μg/ml) or following chondroitinase ABC pretreatment (cABC) (0.5 units/mL). (b) Adhesion of CS2 (white) and CS2KO9 (black bars) IE in the presence of CSA or following anti-CD36 pre-treatment (0.5 μg/ml). (c) Adhesion of E8B (white) and CS2KO9 (black) IE in presence of CSA or following pretreatment with anti-ICAM-1 (10 μg/ml). Adhesion was counted at 40× magnification and expressed as average IE bound per field (+SEM) for at least 3 independent experiments.

    Journal: Malaria Journal

    Article Title: Characterization of VAR2CSA-deficient Plasmodium falciparum-infected erythrocytes selected for adhesion to the BeWo placental cell line

    doi: 10.1186/1475-2875-7-51

    Figure Lengend Snippet: Adhesion to human placental tissue cryosections. Adhesion levels of IE in the intervillous space (IVS), to syncytiotrophoblast (SCT) and over the villus (V) is shown compared to untreated (control) sections present on each slide. (a) Adhesion of CS2 (white bars) and CS2KO9 (black bars) IE in the presence of CSA (100 μg/ml) or following chondroitinase ABC pretreatment (cABC) (0.5 units/mL). (b) Adhesion of CS2 (white) and CS2KO9 (black bars) IE in the presence of CSA or following anti-CD36 pre-treatment (0.5 μg/ml). (c) Adhesion of E8B (white) and CS2KO9 (black) IE in presence of CSA or following pretreatment with anti-ICAM-1 (10 μg/ml). Adhesion was counted at 40× magnification and expressed as average IE bound per field (+SEM) for at least 3 independent experiments.

    Article Snippet: To determine whether CS2KO9 IE which adhered to immobilized ICAM-1 also adhered to ICAM-1 on BeWo cells or placental sections, a blocking antibody to ICAM-1 was used.

    Techniques:

    Effect of Pom on MHC-I (HLA-A, B and C), ICAM and B7-2 mRNA gene expression in BCBL-1 cells induced with butyrate BCBL-1 cells were treated with control (DMSO) or Pom (1 μM) for 24 h followed by treatment with PBS or butyrate for an additional 24 h. Total mRNA was isolated and analyzed for expression levels by real time QT-PCR and was normalized to 18S levels. Shown are the fold changes in mRNA expression for total A . HLA and HLA A, B and C alleles following treatment and B . ICAM-1 and B7-2. Values are the average +/- standard deviation of four independent experiments. *** P

    Journal: Oncotarget

    Article Title: Restoration of immune surface molecules in Kaposi sarcoma-associated herpes virus infected cells by lenalidomide and pomalidomide

    doi: 10.18632/oncotarget.17960

    Figure Lengend Snippet: Effect of Pom on MHC-I (HLA-A, B and C), ICAM and B7-2 mRNA gene expression in BCBL-1 cells induced with butyrate BCBL-1 cells were treated with control (DMSO) or Pom (1 μM) for 24 h followed by treatment with PBS or butyrate for an additional 24 h. Total mRNA was isolated and analyzed for expression levels by real time QT-PCR and was normalized to 18S levels. Shown are the fold changes in mRNA expression for total A . HLA and HLA A, B and C alleles following treatment and B . ICAM-1 and B7-2. Values are the average +/- standard deviation of four independent experiments. *** P

    Article Snippet: Primers for ICAM-1 and B7-2 were from Biorad (ICAM-1: 10025636, qHsaCED0004281) and (B7-2: 10025636, qHsaCED0043530 (Hercules, CA).

    Techniques: Expressing, Isolation, Polymerase Chain Reaction, Standard Deviation

    Restoration of ICAM-1 and B7-2 but not ICAM-3 expression in BCBL-1 cells treated with Pom A . ICAM-1 expression in BCBL-1 cells and in B . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). C . B7-2 expression in BCBL-1 cells and in D . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). E . ICAM-3 expression in BCBL-1 cells and in F . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). The data shows a representative experiment of four independent experiments for A . and C . and two independent experiments for B ., D ., and F . with similar results. The grey shading shows the isotype control.

    Journal: Oncotarget

    Article Title: Restoration of immune surface molecules in Kaposi sarcoma-associated herpes virus infected cells by lenalidomide and pomalidomide

    doi: 10.18632/oncotarget.17960

    Figure Lengend Snippet: Restoration of ICAM-1 and B7-2 but not ICAM-3 expression in BCBL-1 cells treated with Pom A . ICAM-1 expression in BCBL-1 cells and in B . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). C . B7-2 expression in BCBL-1 cells and in D . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). E . ICAM-3 expression in BCBL-1 cells and in F . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). The data shows a representative experiment of four independent experiments for A . and C . and two independent experiments for B ., D ., and F . with similar results. The grey shading shows the isotype control.

    Article Snippet: Primers for ICAM-1 and B7-2 were from Biorad (ICAM-1: 10025636, qHsaCED0004281) and (B7-2: 10025636, qHsaCED0043530 (Hercules, CA).

    Techniques: Expressing, FACS

    Effect of Len on ICAM-1 and B7-2 expression in BCBL-1 cells, effect of Pom on MHC-II expression in BCBL-1 and BJAB cells, and effect of Pom on ICAM-1 and B7-2 in JSC-1 cells A . ICAM-1 expression and B . B7-2 expression in BCBL-1 cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. C . ICAM-1 expression D . B7-2 expression in JSC-1 cells pretreated for 48 h with DMSO vehicle control or Pom (0.2 μM) as determined by FACS. E . MHC-II expression in BCBL-1 cells or F . BJAB cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. The data is representative of two independent experiments in A, one experiment in B-D, and two experiments in E and F. The grey shading shows the isotype control.

    Journal: Oncotarget

    Article Title: Restoration of immune surface molecules in Kaposi sarcoma-associated herpes virus infected cells by lenalidomide and pomalidomide

    doi: 10.18632/oncotarget.17960

    Figure Lengend Snippet: Effect of Len on ICAM-1 and B7-2 expression in BCBL-1 cells, effect of Pom on MHC-II expression in BCBL-1 and BJAB cells, and effect of Pom on ICAM-1 and B7-2 in JSC-1 cells A . ICAM-1 expression and B . B7-2 expression in BCBL-1 cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. C . ICAM-1 expression D . B7-2 expression in JSC-1 cells pretreated for 48 h with DMSO vehicle control or Pom (0.2 μM) as determined by FACS. E . MHC-II expression in BCBL-1 cells or F . BJAB cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. The data is representative of two independent experiments in A, one experiment in B-D, and two experiments in E and F. The grey shading shows the isotype control.

    Article Snippet: Primers for ICAM-1 and B7-2 were from Biorad (ICAM-1: 10025636, qHsaCED0004281) and (B7-2: 10025636, qHsaCED0043530 (Hercules, CA).

    Techniques: Expressing, FACS

    Increased inflammation, ER stress and oxidative stress in aorta of ApoCIIItgLDLR−/− mice comparing to LDLR−/− mice. ( a ) Representative images of Oil Red O (ORO) stained aortic roots and immunohistochemical staining of aortic sinus sections of Mac2, 4HNE and VCAM-1 expression in LDLR−/− and ApoCIIItgLDLR−/− mice. ( b ) Representative Western blot images of VCAM-1 and ICAM-1 protein expression in aortas of LDLR−/− and ApoCIIItgLDLR−/− mice and the protein quantification by densitometry ( n = 4). ( c ) Representative Western blot images of GRP78 protein expression in aortas of LDLR−/− and ApoCIIItgLDLR−/− mice and the protein quantification by densitometry ( n = 4). Values are expressed as mean ± SEM, * p

    Journal: Lipids in Health and Disease

    Article Title: Increased inflammation, endoplasmic reticulum stress and oxidative stress in endothelial and macrophage cells exacerbate atherosclerosis in ApoCIII transgenic mice

    doi: 10.1186/s12944-018-0867-5

    Figure Lengend Snippet: Increased inflammation, ER stress and oxidative stress in aorta of ApoCIIItgLDLR−/− mice comparing to LDLR−/− mice. ( a ) Representative images of Oil Red O (ORO) stained aortic roots and immunohistochemical staining of aortic sinus sections of Mac2, 4HNE and VCAM-1 expression in LDLR−/− and ApoCIIItgLDLR−/− mice. ( b ) Representative Western blot images of VCAM-1 and ICAM-1 protein expression in aortas of LDLR−/− and ApoCIIItgLDLR−/− mice and the protein quantification by densitometry ( n = 4). ( c ) Representative Western blot images of GRP78 protein expression in aortas of LDLR−/− and ApoCIIItgLDLR−/− mice and the protein quantification by densitometry ( n = 4). Values are expressed as mean ± SEM, * p

    Article Snippet: Primary antibody incubations were performed at 4 °C overnight using a 1:1000 dilution for anti-VCAM-1 antibody (ab134047, Abcam), anti-ICAM-1 antibody (ab171123, Abcam), or anti-GRP78 antibody (#3177, Cell Signaling Technology).

    Techniques: Mouse Assay, Staining, Immunohistochemistry, Expressing, Western Blot

    Human CMV infection alters the cell surface expression of key molecules involved in mDC function. (A) Dot plot showing expression of MHC class I molecules on the surface of mock infected (left) or CMV strain TB40/E-infected LC-derived mDCs (right) at day 2 p.i. Cells were stained with a PE-conjugated anti-MHC class I monoclonal antibody ( x axis), as well as with an FITC-conjugated anti-IE1/IE2 monoclonal antibody ( y axis). (B) Flow cytometry analysis of expression levels of MHC class I, MHC class II, CD1a, CD80, CD86, CD83, CD54, CCR7, and CD40 on the surface of mock-infected and CMV strain TB40/E-infected LC-derived mDCs at day 2 p.i. Filled histograms, mock-infected cells; open histograms, TB40/E-infected cells; gray line, isotype controls.

    Journal: Journal of Virology

    Article Title: Susceptibility of Immature and Mature Langerhans Cell-Type Dendritic Cells to Infection and Immunomodulation by Human Cytomegalovirus

    doi: 10.1128/JVI.77.13.7563-7574.2003

    Figure Lengend Snippet: Human CMV infection alters the cell surface expression of key molecules involved in mDC function. (A) Dot plot showing expression of MHC class I molecules on the surface of mock infected (left) or CMV strain TB40/E-infected LC-derived mDCs (right) at day 2 p.i. Cells were stained with a PE-conjugated anti-MHC class I monoclonal antibody ( x axis), as well as with an FITC-conjugated anti-IE1/IE2 monoclonal antibody ( y axis). (B) Flow cytometry analysis of expression levels of MHC class I, MHC class II, CD1a, CD80, CD86, CD83, CD54, CCR7, and CD40 on the surface of mock-infected and CMV strain TB40/E-infected LC-derived mDCs at day 2 p.i. Filled histograms, mock-infected cells; open histograms, TB40/E-infected cells; gray line, isotype controls.

    Article Snippet: CD86 (FITC, clone BU63), HLA-DR (FITC or PE, clone TU36), HLA class I (FITC or PE, clone TU149), CD54 (FITC, clone MEM111), and CD14 (FITC, clone TUK4) antibodies were purchased from Caltag.

    Techniques: Infection, Expressing, Derivative Assay, Staining, Flow Cytometry, Cytometry

    Dynamic analysis of cytoadherence features of eight isolates during the adaptive cultivation. Significant binding was defined as > 5PRBC/mm2, and the final value of bound cells numbers was adjusted in terms of parasitemia of different batches used in the assay. The four purified receptors, CD36, ICAM-1, CSA, and HA were used as immobilized receptors with BSA as negative control. The time points of upregulation of ICAM-1 binding activity were indicated by arrows.

    Journal: PLoS ONE

    Article Title: From In Vivo to In Vitro: Dynamic Analysis of Plasmodium falciparum var Gene Expression Patterns of Patient Isolates during Adaptation to Culture

    doi: 10.1371/journal.pone.0020591

    Figure Lengend Snippet: Dynamic analysis of cytoadherence features of eight isolates during the adaptive cultivation. Significant binding was defined as > 5PRBC/mm2, and the final value of bound cells numbers was adjusted in terms of parasitemia of different batches used in the assay. The four purified receptors, CD36, ICAM-1, CSA, and HA were used as immobilized receptors with BSA as negative control. The time points of upregulation of ICAM-1 binding activity were indicated by arrows.

    Article Snippet: Plastic Petri dishes were coated overnight at 4°C with 1xPBS containing either 1 mg/ml CSA sodium salt from bovine trachea (Sigma), 100 µg/ml HA sodium salt from bovine vitreous humor (Sigma), 10 µg/ml recombinant human CD36 (R & D Systems), 10 µg/ml recombinant human ICAM-1 (R & D Systems) or 1% BSA.

    Techniques: Binding Assay, Purification, Negative Control, Activity Assay