icam-1 Search Results


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  • 94
    Boster Bio intercellular adhesion molecule 1
    Intercellular Adhesion Molecule 1, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher icam 1
    Icam 1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 1915 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam icam 1
    Hyperglycemia induces HSP22 upregulation and endothelial injury in vivo . Type 2 diabetes mellitus (T2DM) mice were induced with a high-fat diet (HFD; 60% of calories from fat) and injected with streptozotocin (STZ; 100 mg/kg) or buffer for 12 weeks (n = 8 per group). A ) Blood glucose concentrations in control, HFD-control and diabetic mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. B ) The body weights of the control, HFD-control and diabetic mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. C ) Representative images of hematoxylin and eosin staining (H E, original magnification ×40). D ) Representative immunohistochemical staining images of <t>ICAM-1,</t> VCAM-1 and HSP22 in aortic sections (original magnification ×40). E ) Quantification of positive staining for ICAM-1 and VCAM-1 in aortic rings. n = 5. F ) Representative images of a gene heat map from a cytokine array. Serum was obtained from each group of mice for a murine cytokine array analysis. Unsupervised hierarchical clustering of genes was performed to generate heat maps showing the genes that were regulated by hyperglycemia (n = 3 per group). G ) Quantification of the fluorescence intensities of cytokine levels in serum. H ) mRNA expression of IL5, IL6, IL13, Mip3α and TGFβ1 in the aorta. I ) Quantification of positive staining for HSP22 in aortic sections. n = 5. J ) mRNA expression of HSP22 in the aorta. * P
    Icam 1, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 1555 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher gene exp icam1 hs00164932 m1
    KFDV infection of HDMECs leads to their activation. a HDMECs were infected with KFDV at an MOI of 10. Mock-infected HDMECs were exposed to the same dose of UV-inactivated KFDV. At 24 and 48 h p.i., mRNA expression of E-selectin, <t>ICAM1,</t> and VCAM1 was analyzed by qRT-PCR and normalized to the expression of housekeeping genes. Fold increase indicates differences in normalized mRNA expression relative to expression in noninfected cells. b Flow cytometry was used to measure the protein levels of E-selectin, VCAM1, and ICAM1 expression in the KFDV-infected HDMECs at 48 h p.i. The production of cell-adhesion molecules is shown in overlapping histograms of relative fluoresce intensity in the analyzed cells; empty histograms with solid lines represent mock-infected (UV-inactivated virus) HDMECs, and gray histograms represent the KFDV-infected cells. c HDMECs were treated with TNF-α (positive control) or mock-infected with UV-inactivated KFDV or infected with KFDV at an MOI of 10 and incubated for 24 and 48 h. After incubation, the adhesion of BCECF–stained leukocytes was measured as described in the Materials and Methods. The leukocyte adhesion index represents the fold change relative to controls (y-axis). d HDMECs grown and fixed on slides at 48 h p.i. were stained with anti-flavivirus envelope (green) and anti-occludin (red) or anti-ZO-1 antibodies and counterstained with DAPI (blue). Bar = 20 µm. e Total RNA from uninfected, mock- and KFDV-infected HDMECs 48 h p.i. was used to determine the fold change in occludin and ZO-1 mRNA expression by qRT-PCR. * p
    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
    KFDV infection of HDMECs leads to their activation. a HDMECs were infected with KFDV at an MOI of 10. Mock-infected HDMECs were exposed to the same dose of UV-inactivated KFDV. At 24 and 48 h p.i., mRNA expression of E-selectin, <t>ICAM1,</t> and VCAM1 was analyzed by qRT-PCR and normalized to the expression of housekeeping genes. Fold increase indicates differences in normalized mRNA expression relative to expression in noninfected cells. b Flow cytometry was used to measure the protein levels of E-selectin, VCAM1, and ICAM1 expression in the KFDV-infected HDMECs at 48 h p.i. The production of cell-adhesion molecules is shown in overlapping histograms of relative fluoresce intensity in the analyzed cells; empty histograms with solid lines represent mock-infected (UV-inactivated virus) HDMECs, and gray histograms represent the KFDV-infected cells. c HDMECs were treated with TNF-α (positive control) or mock-infected with UV-inactivated KFDV or infected with KFDV at an MOI of 10 and incubated for 24 and 48 h. After incubation, the adhesion of BCECF–stained leukocytes was measured as described in the Materials and Methods. The leukocyte adhesion index represents the fold change relative to controls (y-axis). d HDMECs grown and fixed on slides at 48 h p.i. were stained with anti-flavivirus envelope (green) and anti-occludin (red) or anti-ZO-1 antibodies and counterstained with DAPI (blue). Bar = 20 µm. e Total RNA from uninfected, mock- and KFDV-infected HDMECs 48 h p.i. was used to determine the fold change in occludin and ZO-1 mRNA expression by qRT-PCR. * p
    Gene Exp Icam1 Mm00516023 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 408 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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
    Uninfected BM macrophages respond to TNF-α treatment in the presence of infected BM macrophages. Shown is FACS analysis of BM macrophages for surface <t>ICAM-1</t> expression. Results of one representative experiment of six independent experiments are shown.
    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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    Dianova icam 1
    (a) B. henselae Berlin-1 OMPs in the range of 10 pg/ml to 1 μg/ml dose dependently enhanced E-selectin and <t>ICAM-1</t> expression in HUVEC. OMPs were added to cell monolayers in 96-well plates by centrifugation at 1,500 × g . After 8 (E-selectin) or 48 h (ICAM-1) cells were processed for cell surface ELISA. Data are means ± standard errors of the means of three separate experiments. (b) Northern blot showing increase of E-selectin and ICAM-1 mRNA in HUVEC exposed to OMP, TNF-α (10 ng/ml), and LPS (100 ng/ml) after 5 h of stimulation. OMPs were added in a concentration of 500 ng/ml. When indicated, polymyxin B (50 μg/ml) was added 5 min prior to exposure to OMPs or LPS. A representative blot (from one of three independent experiments) is shown.
    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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    96
    Abcam anti icam 1
    (A) Western blot analysis of <t>ICAM-1,</t> GAPDH, p-p38 MAPK and total p38 MAPK in MSCs, EPCs and MSCs + EPCs, with or without IL-1β (25 µ g/ml) or p38 MAPK inhibitor SB203580 (20 µ mol/ml) treatment. Lanes 1–3, normally cultured MSCs, EPCs and MSCs + EPCs groups, respectively; lanes 4–6, IL-1β (25 µ g/ml)-stimulated MSCs, EPCs and MSCs + EPCs groups, respectively; lanes 7–9, p38 MAPK inhibitor SB203580 (20 µ mol/ml)-stimulated MSCs, EPCs and MSCs + EPCs groups, respectively. (B) ICAM-1/GAPDH and (C) p-p38 MAPK/total-p38 MAPK IOD relative values were determined. Data are presented as the means ± standard deviation of three independent experiments. * P
    Anti Icam 1, supplied by Abcam, used in various techniques. Bioz Stars score: 96/100, based on 256 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Becton Dickinson icam 1
    2′- O -methyl modification of the 736 sense strand eliminates TNFR1 knockdown. ( A ) Hybrid 736 siRNA duplexes were prepared by annealing unmodified 736 RNA oligos (sense or antisense) with complementary RNA oligos modified by 2′- O -methylation, (such hybrid duplexes are indicated as 736/S or 736/AS). Dual modified duplexes (736/S+AS) and wild-type 736 (736/WT) were also prepared. 2′- O -Me modified bases are in bold and underlined. ( B ) HUVEC were mock-transfected or transfected with 10 nM LFA-3, an irrelevant siRNA, 736/WT, 736/S, 736/AS or 736/S + AS siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for <t>ICAM-1</t> and E-selectin and analyzed by flow cytometry. Corrected MFIs were converted to ‘% Remaining’ relative to mock expression. ( C ) Hybrid siRNA-transfected HUVEC lysates were analyzed by western blot for the expression of TNFR1 and β-actin. Representative of one of two experiments with similar results.
    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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    94
    Thermo Fisher anti icam 1
    Cell surface expression of LFA-1 and <t>ICAM-1</t> on Jurkat cells. FACS analysis of expression of CD18 (beta subunit of LFA-1) and ICAM-1 on Jurkat cells expressing ITK (no shRNA, n.t. shRNA) or not expressing ITK (258 shRNA, 614 shRNA) by using anti-CD18-FITC antibody and anti-ICAM-FITC. Filled histograms represent the isotype control. All figures show one representative experiment out of three repetitions.
    Anti Icam 1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 166 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    icam1  (Abcam)
    92
    Abcam icam1
    Regulation of <t>ICAM1</t> through ALK stimulation. ICAM1 expression in nasal biopsies from patients with CRSwNP and healthy controls (n = 6–7) ( a ). ICAM1 expression on cultured epithelial cells (n = 5) ( b ) or stimulated with TGF-β1 ( c ), Activin A ( d ), BMP4 ( e ) or Activin B ( f ) for 24 h (n = 3). White bars (Control epithelial cells), gray bars (Polyp epithelial cells). Values: mean ± SEM. Friedman-test with Dunn’s post-test, was used for comparisons of more than two data sets. An unpaired t- test was used to compare two sets of data.
    Icam1, supplied by Abcam, used in various techniques. Bioz Stars score: 92/100, based on 174 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    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
    Icam 1, supplied by USCN Life, used in various techniques. Bioz Stars score: 92/100, based on 78 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems mouse icam 1 cd54 antibody
    RelB overexpression reduces cigarette smoke–induced <t>ICAM-1</t> expression in mouse lungs. Mice were treated with either the RelB or control virus (two doses of 5 × 10 8 plaque-forming units per mouse delivered 24 hours apart) and exposed to
    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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    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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    Bio-Rad 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 Bio-Rad, used in various techniques. Bioz Stars score: 93/100, based on 395 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    GeneTex icam 1
    R1R2 decreases TNF-α-induced monocyte U937 cell adhesion to HUVECs and transendothelial migration and reduces <t>ICAM-1</t> and VCAM-1 levels. (A) HUVECs were pretreated with R1R2 or scramble peptide before treatment with TNF-α (10ng/ml) for 6 hours in the continued presence of R1R2 or scrambled peptide. Calcein-AM labeled U937 monocyte adhesion to TNF-α HUVECs was quantitated by fluorescence intensity. Microscopic images showing U937 monocytes adhering to HUVECs as assessed by in vitro adhesion assay. (B) Calcein-AM-labeled U937 monocytes transmigrated through TNF-α-treated HUVECs. (C) Western blot analysis of ICAM-1 and VCAM-1 expression in TNF-α-treated HUVECs. * indicates p
    Icam 1, supplied by GeneTex, used in various techniques. Bioz Stars score: 92/100, based on 104 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems recombinant human icam 1
    Affinity and antigen-density dependent activation of Jurkat CAR T cells in vitro . ( a ) Top, histograms depicting 8 μm latex beads coupled with known amounts of R6.5 antibody conjugated with cy5.5 (10 3 –10 7 antibodies per bead). The level of shift after incubation with R6.5 (black) from non-labeled (grey) was used to estimate <t>ICAM-1</t> density in each indicated target cell line. 8505 C/-ICAM-1; 8505 C cells with ICAM-1 gene inactivation by CRISPR/Cas9. 8505 C/LPS, 8505 C cells were incubated with LPS to induce overexpression of ICAM-1. ( b ) CD25 expression in Jurkat CAR T cells (WT, F292A, F292G, and TM) after co-incubation with different target cell lines for 24 h (n = 3–4). p
    Recombinant Human Icam 1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 99/100, based on 108 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Abcam anti icam1
    Representative immunohistochemical staining against ETR in skin equivalents topically treated with ETR dissolved in PBS (a) or encapsulated in tNG_pNIPAM (b) or tNG_tPG (c). Images show pseudo coloured ETR temperature staining (scale and direction of increasing signal intensity shown on the right) overlaid onto differential interference contrast (DIC) images, onto which the boundaries between the stratum corneum / viable epidermis (upper) and the viable epidermis / dermis (lower) have been marked (scale bar = 50 µm). Protein levels of TNFα, TSLP and <t>ICAM1</t> in TNFα treated skin equivalents (black) calculated as a percentage of normal skin equivalents (grey) (d). Protein levels of TNFα (e), TSLP (f) and ICAM1 (g) in TNFα treated skin equivalents following treatment with empty (grey) or ETR loaded (black) tNGs or PBS. Values are expressed as a percentage of TNFα treated controls. Insets show representative western blots from the protein of interest, above, and β actin, below. Dashed lines indicate mean protein levels found in untreated, normal skin equivalents. Statistical differences from the normal controls (d) or TNFα treated controls (e-f) were calculated by Student's t -test (n = 3, error bars = SEM, * = p ≤ 0.05).
    Anti Icam1, supplied by Abcam, used in various techniques. Bioz Stars score: 95/100, based on 81 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher gene exp icam1 rn00564227 m1
    Representative immunohistochemical staining against ETR in skin equivalents topically treated with ETR dissolved in PBS (a) or encapsulated in tNG_pNIPAM (b) or tNG_tPG (c). Images show pseudo coloured ETR temperature staining (scale and direction of increasing signal intensity shown on the right) overlaid onto differential interference contrast (DIC) images, onto which the boundaries between the stratum corneum / viable epidermis (upper) and the viable epidermis / dermis (lower) have been marked (scale bar = 50 µm). Protein levels of TNFα, TSLP and <t>ICAM1</t> in TNFα treated skin equivalents (black) calculated as a percentage of normal skin equivalents (grey) (d). Protein levels of TNFα (e), TSLP (f) and ICAM1 (g) in TNFα treated skin equivalents following treatment with empty (grey) or ETR loaded (black) tNGs or PBS. Values are expressed as a percentage of TNFα treated controls. Insets show representative western blots from the protein of interest, above, and β actin, below. Dashed lines indicate mean protein levels found in untreated, normal skin equivalents. Statistical differences from the normal controls (d) or TNFα treated controls (e-f) were calculated by Student's t -test (n = 3, error bars = SEM, * = p ≤ 0.05).
    Gene Exp Icam1 Rn00564227 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 98/100, based on 74 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems rat icam 1 cd54 antibody
    Representative immunohistochemical staining against ETR in skin equivalents topically treated with ETR dissolved in PBS (a) or encapsulated in tNG_pNIPAM (b) or tNG_tPG (c). Images show pseudo coloured ETR temperature staining (scale and direction of increasing signal intensity shown on the right) overlaid onto differential interference contrast (DIC) images, onto which the boundaries between the stratum corneum / viable epidermis (upper) and the viable epidermis / dermis (lower) have been marked (scale bar = 50 µm). Protein levels of TNFα, TSLP and <t>ICAM1</t> in TNFα treated skin equivalents (black) calculated as a percentage of normal skin equivalents (grey) (d). Protein levels of TNFα (e), TSLP (f) and ICAM1 (g) in TNFα treated skin equivalents following treatment with empty (grey) or ETR loaded (black) tNGs or PBS. Values are expressed as a percentage of TNFα treated controls. Insets show representative western blots from the protein of interest, above, and β actin, below. Dashed lines indicate mean protein levels found in untreated, normal skin equivalents. Statistical differences from the normal controls (d) or TNFα treated controls (e-f) were calculated by Student's t -test (n = 3, error bars = SEM, * = p ≤ 0.05).
    Rat Icam 1 Cd54 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 99/100, based on 68 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abnova icam 1
    Del-1 inhibits <t>ICAM-1-dependent</t> chemokine production by neutrophils. (a)–(c) ATRA-differentiated HL-60 neutrophils were cultured for 24 hours on plates coated with Fc protein control, ICAM-1-Fc, or Del-1-Fc, and induction of release of CCL3 (a), CXCL2 (b), and TNF (c) was assayed by ELISA. (d)-(e) ATRA-differentiated HL-60 neutrophils were cultured for 24 hours on ICAM-1-Fc-coated plates in the presence of the indicated concentrations of soluble Del-1, and induction of release of CCL3 (d) and CXCL2 (e) was assayed by ELISA. (f)-(g) ATRA-differentiated HL-60 neutrophils were stimulated for 24 hours with 1 μ g/mL Pam 3 CSK 4 or 0.1 μ g/mL LPS, in the absence or presence of the indicated concentrations of Del-1, and induction of release of CCL3 (f) and CXCL2 (g) was assayed by ELISA. Data are means ± SD ((a)–(e), n ≥ 4 and (f)-(g), n = 2 sets of HL-60 cells). * P
    Icam 1, supplied by Abnova, used in various techniques. Bioz Stars score: 92/100, based on 33 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    N/A
    This gene encodes a cell surface glycoprotein which is typically expressed on endothelial cells and cells of the immune system It binds to integrins of type CD11a CD18 or CD11b
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    The ICAM 1 CD54 Recombinant Protein Antigen from Novus Biologicals is derived from E coli The ICAM 1 CD54 Recombinant Protein Antigen has been validated for the following applications Antibody
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    Human ICAM 1 AccuSignal ELISA Kit KOA0187
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    Rat ICAM 1 AccuSignal ELISA Kit KOA0189
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    Image Search Results


    Hyperglycemia induces HSP22 upregulation and endothelial injury in vivo . Type 2 diabetes mellitus (T2DM) mice were induced with a high-fat diet (HFD; 60% of calories from fat) and injected with streptozotocin (STZ; 100 mg/kg) or buffer for 12 weeks (n = 8 per group). A ) Blood glucose concentrations in control, HFD-control and diabetic mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. B ) The body weights of the control, HFD-control and diabetic mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. C ) Representative images of hematoxylin and eosin staining (H E, original magnification ×40). D ) Representative immunohistochemical staining images of ICAM-1, VCAM-1 and HSP22 in aortic sections (original magnification ×40). E ) Quantification of positive staining for ICAM-1 and VCAM-1 in aortic rings. n = 5. F ) Representative images of a gene heat map from a cytokine array. Serum was obtained from each group of mice for a murine cytokine array analysis. Unsupervised hierarchical clustering of genes was performed to generate heat maps showing the genes that were regulated by hyperglycemia (n = 3 per group). G ) Quantification of the fluorescence intensities of cytokine levels in serum. H ) mRNA expression of IL5, IL6, IL13, Mip3α and TGFβ1 in the aorta. I ) Quantification of positive staining for HSP22 in aortic sections. n = 5. J ) mRNA expression of HSP22 in the aorta. * P

    Journal: Redox Biology

    Article Title: HSP22 suppresses diabetes-induced endothelial injury by inhibiting mitochondrial reactive oxygen species formation

    doi: 10.1016/j.redox.2018.101095

    Figure Lengend Snippet: Hyperglycemia induces HSP22 upregulation and endothelial injury in vivo . Type 2 diabetes mellitus (T2DM) mice were induced with a high-fat diet (HFD; 60% of calories from fat) and injected with streptozotocin (STZ; 100 mg/kg) or buffer for 12 weeks (n = 8 per group). A ) Blood glucose concentrations in control, HFD-control and diabetic mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. B ) The body weights of the control, HFD-control and diabetic mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. C ) Representative images of hematoxylin and eosin staining (H E, original magnification ×40). D ) Representative immunohistochemical staining images of ICAM-1, VCAM-1 and HSP22 in aortic sections (original magnification ×40). E ) Quantification of positive staining for ICAM-1 and VCAM-1 in aortic rings. n = 5. F ) Representative images of a gene heat map from a cytokine array. Serum was obtained from each group of mice for a murine cytokine array analysis. Unsupervised hierarchical clustering of genes was performed to generate heat maps showing the genes that were regulated by hyperglycemia (n = 3 per group). G ) Quantification of the fluorescence intensities of cytokine levels in serum. H ) mRNA expression of IL5, IL6, IL13, Mip3α and TGFβ1 in the aorta. I ) Quantification of positive staining for HSP22 in aortic sections. n = 5. J ) mRNA expression of HSP22 in the aorta. * P

    Article Snippet: Primary antibodies for the immunohistochemistry study (HSP22 (ab151552, rabbit monoclonal, at 1:50), ICAM-1 (ab119871, rat monoclonal, at 1:200), and VCAM-1 (ab134047, rabbit monoclonal, at 1:200)) were acquired from Abcam (MA, USA).

    Techniques: In Vivo, Mouse Assay, Injection, Staining, Immunohistochemistry, Fluorescence, Expressing

    HSP22 reduces diabetes-induced endothelial injury in vivo . Diabetes was induced in wild-type (WT) and transgenic (TG) mice by HFD adjuvanted with STZ injection for 12 weeks (n = 8 per group). A ) Blood glucose concentrations in the WT-control, TG-control, WT-diabetic and TG-diabetic mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. B ) The body weights of the WT-control, TG-control, WT-diabetes and TG-diabetes mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. C ) Representative images of H E staining (original magnification ×40). D ) Representative immunohistochemical staining images of HSP22, ICAM-1 and VCAM-1 in aortic sections (original magnification ×40). E ) Quantification of positive staining for HSP22 in aortic sections. n = 5. F ) mRNA expression of HSP22 in the aorta. G ) Quantification of positive staining for ICAM-1 and VCAM-1 in aortic rings. n = 5. H ) mRNA expression of IL5, IL6, IL13, Mip3α and TGFβ1 in the aorta. * P

    Journal: Redox Biology

    Article Title: HSP22 suppresses diabetes-induced endothelial injury by inhibiting mitochondrial reactive oxygen species formation

    doi: 10.1016/j.redox.2018.101095

    Figure Lengend Snippet: HSP22 reduces diabetes-induced endothelial injury in vivo . Diabetes was induced in wild-type (WT) and transgenic (TG) mice by HFD adjuvanted with STZ injection for 12 weeks (n = 8 per group). A ) Blood glucose concentrations in the WT-control, TG-control, WT-diabetic and TG-diabetic mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. B ) The body weights of the WT-control, TG-control, WT-diabetes and TG-diabetes mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. C ) Representative images of H E staining (original magnification ×40). D ) Representative immunohistochemical staining images of HSP22, ICAM-1 and VCAM-1 in aortic sections (original magnification ×40). E ) Quantification of positive staining for HSP22 in aortic sections. n = 5. F ) mRNA expression of HSP22 in the aorta. G ) Quantification of positive staining for ICAM-1 and VCAM-1 in aortic rings. n = 5. H ) mRNA expression of IL5, IL6, IL13, Mip3α and TGFβ1 in the aorta. * P

    Article Snippet: Primary antibodies for the immunohistochemistry study (HSP22 (ab151552, rabbit monoclonal, at 1:50), ICAM-1 (ab119871, rat monoclonal, at 1:200), and VCAM-1 (ab134047, rabbit monoclonal, at 1:200)) were acquired from Abcam (MA, USA).

    Techniques: In Vivo, Transgenic Assay, Mouse Assay, Injection, Staining, Immunohistochemistry, Expressing

    HSP22 deficiency exacerbates diabetes-induced endothelial injury in vivo . Diabetes was induced in wild-type (WT) and knockout (KO) mice by HFD adjuvanted with STZ injection for 12 weeks (n = 8 per group). A ) Blood glucose concentrations in the WT-control, KO-control, WT-diabetes and KO-diabetes mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. B ) The body weights of the WT-control, KO-control, WT-diabetes and KO-diabetes mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. C ) Representative images of H E (original magnification ×40). D ) Representative immunohistochemical staining images of HSP22, ICAM-1 and VCAM-1 in aortic sections (original magnification ×40). E ) Quantification of positive staining for HSP22 in aortic sections. n = 5. F ) mRNA expression of HSP22 in the aorta. G ) Quantification of positive staining for ICAM-1 and VCAM-1 in aortic sections. n = 5. H ) mRNA expression of IL5, IL6, IL13, Mip3α and TGFβ1 in the aorta. * P

    Journal: Redox Biology

    Article Title: HSP22 suppresses diabetes-induced endothelial injury by inhibiting mitochondrial reactive oxygen species formation

    doi: 10.1016/j.redox.2018.101095

    Figure Lengend Snippet: HSP22 deficiency exacerbates diabetes-induced endothelial injury in vivo . Diabetes was induced in wild-type (WT) and knockout (KO) mice by HFD adjuvanted with STZ injection for 12 weeks (n = 8 per group). A ) Blood glucose concentrations in the WT-control, KO-control, WT-diabetes and KO-diabetes mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. B ) The body weights of the WT-control, KO-control, WT-diabetes and KO-diabetes mice were measured at baseline and 4, 8, and 12 weeks after diabetes induction. C ) Representative images of H E (original magnification ×40). D ) Representative immunohistochemical staining images of HSP22, ICAM-1 and VCAM-1 in aortic sections (original magnification ×40). E ) Quantification of positive staining for HSP22 in aortic sections. n = 5. F ) mRNA expression of HSP22 in the aorta. G ) Quantification of positive staining for ICAM-1 and VCAM-1 in aortic sections. n = 5. H ) mRNA expression of IL5, IL6, IL13, Mip3α and TGFβ1 in the aorta. * P

    Article Snippet: Primary antibodies for the immunohistochemistry study (HSP22 (ab151552, rabbit monoclonal, at 1:50), ICAM-1 (ab119871, rat monoclonal, at 1:200), and VCAM-1 (ab134047, rabbit monoclonal, at 1:200)) were acquired from Abcam (MA, USA).

    Techniques: In Vivo, Knock-Out, Mouse Assay, Injection, Immunohistochemistry, Staining, Expressing

    HSP22 deficiency offsets MitoTEMPO-inhibited endothelial injury under hyperglycemic conditions in vitro . HUVECs were transfected with negative control siRNA (NC siRNA) or HSP22 siRNA for 48 h and then treated with high glucose with/without MitoTEMPO (1 μM) for 24 h. A ) Cells in 96-well plates were stained with Cell Counting Kit-8 (CCK8) to evaluate cell viability. n = 3. B ) Cytotoxicity was measured by LDH release in the cell media. n = 3. C ) Adhesion of nonstimulated PBMCs to stimulated HUVECs was quantified. n = 3. D ) mRNA expression of ICAM-1 and VCAM-1 was determined by RT-PCR. n = 3. E ) Endothelial cell activation-related cytokines were examined by RT-PCR. n = 3. * P

    Journal: Redox Biology

    Article Title: HSP22 suppresses diabetes-induced endothelial injury by inhibiting mitochondrial reactive oxygen species formation

    doi: 10.1016/j.redox.2018.101095

    Figure Lengend Snippet: HSP22 deficiency offsets MitoTEMPO-inhibited endothelial injury under hyperglycemic conditions in vitro . HUVECs were transfected with negative control siRNA (NC siRNA) or HSP22 siRNA for 48 h and then treated with high glucose with/without MitoTEMPO (1 μM) for 24 h. A ) Cells in 96-well plates were stained with Cell Counting Kit-8 (CCK8) to evaluate cell viability. n = 3. B ) Cytotoxicity was measured by LDH release in the cell media. n = 3. C ) Adhesion of nonstimulated PBMCs to stimulated HUVECs was quantified. n = 3. D ) mRNA expression of ICAM-1 and VCAM-1 was determined by RT-PCR. n = 3. E ) Endothelial cell activation-related cytokines were examined by RT-PCR. n = 3. * P

    Article Snippet: Primary antibodies for the immunohistochemistry study (HSP22 (ab151552, rabbit monoclonal, at 1:50), ICAM-1 (ab119871, rat monoclonal, at 1:200), and VCAM-1 (ab134047, rabbit monoclonal, at 1:200)) were acquired from Abcam (MA, USA).

    Techniques: In Vitro, Transfection, Negative Control, Staining, Cell Counting, Expressing, Reverse Transcription Polymerase Chain Reaction, Activation Assay

    Transient ligation induces a persistent loss of ACTA2 protein. (A) representative ICAM-1 and ACTA2 stainings of transiently ligated carotid arteries analyzed after 24h (20 min transient ligation) or 28 days (1h transient ligation). Scale Bar equals 100μm. (B) Quantification of ACTA2 positive media (n = 3–4 per time point) (C) Quantification of ICAM-1 positive media (n = 3–4 per time point). Statistical analysis was performed using a one-way analysis of variance with Tukey’s multiple comparison post hoc test.

    Journal: PLoS ONE

    Article Title: Hypoxia/reperfusion predisposes to atherosclerosis

    doi: 10.1371/journal.pone.0205067

    Figure Lengend Snippet: Transient ligation induces a persistent loss of ACTA2 protein. (A) representative ICAM-1 and ACTA2 stainings of transiently ligated carotid arteries analyzed after 24h (20 min transient ligation) or 28 days (1h transient ligation). Scale Bar equals 100μm. (B) Quantification of ACTA2 positive media (n = 3–4 per time point) (C) Quantification of ICAM-1 positive media (n = 3–4 per time point). Statistical analysis was performed using a one-way analysis of variance with Tukey’s multiple comparison post hoc test.

    Article Snippet: For immunofluorescence, the following antibodies were used at indicated concentrations: anti-ACTA2 (Abcam, ab21027) (1:1000), anti-ICAM-1 antibody [YN1/1.7.4] (Abcam, ab119871) (1:200).

    Techniques: Ligation

    KFDV infection of HDMECs leads to their activation. a HDMECs were infected with KFDV at an MOI of 10. Mock-infected HDMECs were exposed to the same dose of UV-inactivated KFDV. At 24 and 48 h p.i., mRNA expression of E-selectin, ICAM1, and VCAM1 was analyzed by qRT-PCR and normalized to the expression of housekeeping genes. Fold increase indicates differences in normalized mRNA expression relative to expression in noninfected cells. b Flow cytometry was used to measure the protein levels of E-selectin, VCAM1, and ICAM1 expression in the KFDV-infected HDMECs at 48 h p.i. The production of cell-adhesion molecules is shown in overlapping histograms of relative fluoresce intensity in the analyzed cells; empty histograms with solid lines represent mock-infected (UV-inactivated virus) HDMECs, and gray histograms represent the KFDV-infected cells. c HDMECs were treated with TNF-α (positive control) or mock-infected with UV-inactivated KFDV or infected with KFDV at an MOI of 10 and incubated for 24 and 48 h. After incubation, the adhesion of BCECF–stained leukocytes was measured as described in the Materials and Methods. The leukocyte adhesion index represents the fold change relative to controls (y-axis). d HDMECs grown and fixed on slides at 48 h p.i. were stained with anti-flavivirus envelope (green) and anti-occludin (red) or anti-ZO-1 antibodies and counterstained with DAPI (blue). Bar = 20 µm. e Total RNA from uninfected, mock- and KFDV-infected HDMECs 48 h p.i. was used to determine the fold change in occludin and ZO-1 mRNA expression by qRT-PCR. * p

    Journal: Emerging Microbes & Infections

    Article Title: Kyasanur Forest disease virus infection activates human vascular endothelial cells and monocyte-derived dendritic cells

    doi: 10.1038/s41426-018-0177-z

    Figure Lengend Snippet: KFDV infection of HDMECs leads to their activation. a HDMECs were infected with KFDV at an MOI of 10. Mock-infected HDMECs were exposed to the same dose of UV-inactivated KFDV. At 24 and 48 h p.i., mRNA expression of E-selectin, ICAM1, and VCAM1 was analyzed by qRT-PCR and normalized to the expression of housekeeping genes. Fold increase indicates differences in normalized mRNA expression relative to expression in noninfected cells. b Flow cytometry was used to measure the protein levels of E-selectin, VCAM1, and ICAM1 expression in the KFDV-infected HDMECs at 48 h p.i. The production of cell-adhesion molecules is shown in overlapping histograms of relative fluoresce intensity in the analyzed cells; empty histograms with solid lines represent mock-infected (UV-inactivated virus) HDMECs, and gray histograms represent the KFDV-infected cells. c HDMECs were treated with TNF-α (positive control) or mock-infected with UV-inactivated KFDV or infected with KFDV at an MOI of 10 and incubated for 24 and 48 h. After incubation, the adhesion of BCECF–stained leukocytes was measured as described in the Materials and Methods. The leukocyte adhesion index represents the fold change relative to controls (y-axis). d HDMECs grown and fixed on slides at 48 h p.i. were stained with anti-flavivirus envelope (green) and anti-occludin (red) or anti-ZO-1 antibodies and counterstained with DAPI (blue). Bar = 20 µm. e Total RNA from uninfected, mock- and KFDV-infected HDMECs 48 h p.i. was used to determine the fold change in occludin and ZO-1 mRNA expression by qRT-PCR. * p

    Article Snippet: PCR was performed using predeveloped TaqMan Assay Reagents [Assay IDs: ICAM-1 (Hs00164932_m1), VCAM-1 (Hs01003372_m1), SELE (Hs00174057_m1), occludin (Hs00170162_m1), and zonula occludens-1 (ZO-1/TJP1; Hs01551876_m1)] and TaqMan Gene Expression Master Mix (Applied Biosystems) on a LightCycler 480 II with a 96-well plate block (Roche, UK).

    Techniques: Infection, Activation Assay, Expressing, Quantitative RT-PCR, Flow Cytometry, Cytometry, Positive Control, Incubation, Staining

    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

    Uninfected BM macrophages respond to TNF-α treatment in the presence of infected BM macrophages. Shown is FACS analysis of BM macrophages for surface ICAM-1 expression. Results of one representative experiment of six independent experiments are shown.

    Journal: Journal of Virology

    Article Title: Murine Cytomegalovirus Infection Inhibits Tumor Necrosis Factor Alpha Responses in Primary Macrophages

    doi: 10.1128/JVI.77.18.10125-10130.2003

    Figure Lengend Snippet: Uninfected BM macrophages respond to TNF-α treatment in the presence of infected BM macrophages. Shown is FACS analysis of BM macrophages for surface ICAM-1 expression. Results of one representative experiment of six independent experiments are shown.

    Article Snippet: MCMV inhibition of TNF-α-induced ICAM-1 expression required live virus, since UV-inactivated MCMV did not block TNF-α induction of ICAM-1 and was specific to ICAM-1, as MCMV infection does not affect the surface expression of IFNGR1 ( ).

    Techniques: Infection, FACS, Expressing

    MCMV IE and/or E genes block TNF-α-induced ICAM-1 expression. (a) FACS analysis of BM macrophages for surface ICAM-1 expression. (b) BM macrophages were infected and stimulated as done for panel a with the addition of phosphonoacetic acid (PAA) treatment. Isotype control is represented by filled histograms in panels a and b. Results of one representative experiment of three independent experiments are shown.

    Journal: Journal of Virology

    Article Title: Murine Cytomegalovirus Infection Inhibits Tumor Necrosis Factor Alpha Responses in Primary Macrophages

    doi: 10.1128/JVI.77.18.10125-10130.2003

    Figure Lengend Snippet: MCMV IE and/or E genes block TNF-α-induced ICAM-1 expression. (a) FACS analysis of BM macrophages for surface ICAM-1 expression. (b) BM macrophages were infected and stimulated as done for panel a with the addition of phosphonoacetic acid (PAA) treatment. Isotype control is represented by filled histograms in panels a and b. Results of one representative experiment of three independent experiments are shown.

    Article Snippet: MCMV inhibition of TNF-α-induced ICAM-1 expression required live virus, since UV-inactivated MCMV did not block TNF-α induction of ICAM-1 and was specific to ICAM-1, as MCMV infection does not affect the surface expression of IFNGR1 ( ).

    Techniques: Blocking Assay, Expressing, FACS, Infection

    MCMV inhibits TNF-α-induced transcription and NF-kB translocation in BM macrophages. (a) qRT-PCR analysis was performed to quantitate TNF-α-induced TRAF1 and ICAM-1 transcripts. The mean and standard error of the mean are shown from four independent experiments. (b) Confocal immunofluorescence studies were performed to monitor TNF-α-induced NF-κB nuclear localization in the presence or absence of MCMV infection. Results of one of three independent experiments are shown.

    Journal: Journal of Virology

    Article Title: Murine Cytomegalovirus Infection Inhibits Tumor Necrosis Factor Alpha Responses in Primary Macrophages

    doi: 10.1128/JVI.77.18.10125-10130.2003

    Figure Lengend Snippet: MCMV inhibits TNF-α-induced transcription and NF-kB translocation in BM macrophages. (a) qRT-PCR analysis was performed to quantitate TNF-α-induced TRAF1 and ICAM-1 transcripts. The mean and standard error of the mean are shown from four independent experiments. (b) Confocal immunofluorescence studies were performed to monitor TNF-α-induced NF-κB nuclear localization in the presence or absence of MCMV infection. Results of one of three independent experiments are shown.

    Article Snippet: MCMV inhibition of TNF-α-induced ICAM-1 expression required live virus, since UV-inactivated MCMV did not block TNF-α induction of ICAM-1 and was specific to ICAM-1, as MCMV infection does not affect the surface expression of IFNGR1 ( ).

    Techniques: Translocation Assay, Quantitative RT-PCR, Immunofluorescence, Infection

    (a) B. henselae Berlin-1 OMPs in the range of 10 pg/ml to 1 μg/ml dose dependently enhanced E-selectin and ICAM-1 expression in HUVEC. OMPs were added to cell monolayers in 96-well plates by centrifugation at 1,500 × g . After 8 (E-selectin) or 48 h (ICAM-1) cells were processed for cell surface ELISA. Data are means ± standard errors of the means of three separate experiments. (b) Northern blot showing increase of E-selectin and ICAM-1 mRNA in HUVEC exposed to OMP, TNF-α (10 ng/ml), and LPS (100 ng/ml) after 5 h of stimulation. OMPs were added in a concentration of 500 ng/ml. When indicated, polymyxin B (50 μg/ml) was added 5 min prior to exposure to OMPs or LPS. A representative blot (from one of three independent experiments) is shown.

    Journal: Infection and Immunity

    Article Title: Bartonella henselae Induces NF-?B-Dependent Upregulation of Adhesion Molecules in Cultured Human Endothelial Cells: Possible Role of Outer Membrane Proteins as Pathogenic Factors

    doi: 10.1128/IAI.69.8.5088-5097.2001

    Figure Lengend Snippet: (a) B. henselae Berlin-1 OMPs in the range of 10 pg/ml to 1 μg/ml dose dependently enhanced E-selectin and ICAM-1 expression in HUVEC. OMPs were added to cell monolayers in 96-well plates by centrifugation at 1,500 × g . After 8 (E-selectin) or 48 h (ICAM-1) cells were processed for cell surface ELISA. Data are means ± standard errors of the means of three separate experiments. (b) Northern blot showing increase of E-selectin and ICAM-1 mRNA in HUVEC exposed to OMP, TNF-α (10 ng/ml), and LPS (100 ng/ml) after 5 h of stimulation. OMPs were added in a concentration of 500 ng/ml. When indicated, polymyxin B (50 μg/ml) was added 5 min prior to exposure to OMPs or LPS. A representative blot (from one of three independent experiments) is shown.

    Article Snippet: Purified freeze-dried monoclonal antibodies (MAbs) directed against E-selectin (1.2B6), vascular cell adhesion molecule 1 (VCAM-1) (1G11), and ICAM-1 (15.2) were from Dianova (Hamburg, Germany), and horseradish peroxidase-conjugated polyclonal sheep anti-mouse immunoglobulin G (IgG) antibodies (Abs) were from Amersham Pharmacia (Freiburg, Germany).

    Techniques: Expressing, Centrifugation, Enzyme-linked Immunosorbent Assay, Northern Blot, Concentration Assay

    PMN rolling and adhesion on Bartonella- exposed HUVEC under flow at a shear rate of 1 dyne/cm 2 . Bacteria were centrifuged on endothelial cells in four-well plates containing rectangular coverslips. After 8 h coverslips were processed for a laminar-flow adhesion assay. PMN (3 × 10 6 per ml) were injected into the flow system and perfused over endothelial cell monolayers for 5 min using a high-precision syringe pump. When indicated, cells were preincubated with Abs against E-selectin, ICAM-1, or VCAM-1 120 min before measurement. TNF-α (20 ng/ml) was used as a positive control. Rolling PMN (for a definition see Materials and Methods) were counted over a 3-min observation period. Adherent PMN were determined by counting 10 to 12 random high-power fields (see Materials and Methods). B. henselae Berlin-1 was almost as effective as TNF-α. Note that PMN rolling and adhesion were almost completely blocked by an anti-E-selectin MAb. Data are means ± standard errors of the means of three separate experiments.

    Journal: Infection and Immunity

    Article Title: Bartonella henselae Induces NF-?B-Dependent Upregulation of Adhesion Molecules in Cultured Human Endothelial Cells: Possible Role of Outer Membrane Proteins as Pathogenic Factors

    doi: 10.1128/IAI.69.8.5088-5097.2001

    Figure Lengend Snippet: PMN rolling and adhesion on Bartonella- exposed HUVEC under flow at a shear rate of 1 dyne/cm 2 . Bacteria were centrifuged on endothelial cells in four-well plates containing rectangular coverslips. After 8 h coverslips were processed for a laminar-flow adhesion assay. PMN (3 × 10 6 per ml) were injected into the flow system and perfused over endothelial cell monolayers for 5 min using a high-precision syringe pump. When indicated, cells were preincubated with Abs against E-selectin, ICAM-1, or VCAM-1 120 min before measurement. TNF-α (20 ng/ml) was used as a positive control. Rolling PMN (for a definition see Materials and Methods) were counted over a 3-min observation period. Adherent PMN were determined by counting 10 to 12 random high-power fields (see Materials and Methods). B. henselae Berlin-1 was almost as effective as TNF-α. Note that PMN rolling and adhesion were almost completely blocked by an anti-E-selectin MAb. Data are means ± standard errors of the means of three separate experiments.

    Article Snippet: Purified freeze-dried monoclonal antibodies (MAbs) directed against E-selectin (1.2B6), vascular cell adhesion molecule 1 (VCAM-1) (1G11), and ICAM-1 (15.2) were from Dianova (Hamburg, Germany), and horseradish peroxidase-conjugated polyclonal sheep anti-mouse immunoglobulin G (IgG) antibodies (Abs) were from Amersham Pharmacia (Freiburg, Germany).

    Techniques: Flow Cytometry, Cell Adhesion Assay, Injection, Positive Control

    (a) Enhanced expression of E-selectin and ICAM-1 in B. henselae- infected HUVEC. Bacteria were added to HUVEC monolayers in 96-well plates by centrifugation at 1,500 × g in a bacteria-to-cell ratio of 50:1. After 2 h plates were washed three times with fresh medium. After incubation for another 2 to 144 h, cells were processed for E-selectin or ICAM-1 cell surface ELISA. Note that E-selectin expression peaked at 7 to 12 h, while ICAM-1 increased up to 144 h. Data are means ± standard errors of the means of four separate experiments. (b) Northern blot showing increase of E-selectin and ICAM-1 mRNA in B. henselae- infected HUVEC. Total endothelial RNA was isolated, and levels of E-selectin-, ICAM-1, and GAPDH mRNA were quantitated. Note different time patterns of mRNA expression after B. henselae infection for E-selectin and ICAM-1 and the remarkably long upregulation of ICAM-1. A representative gel (of four independent experiments) is shown.

    Journal: Infection and Immunity

    Article Title: Bartonella henselae Induces NF-?B-Dependent Upregulation of Adhesion Molecules in Cultured Human Endothelial Cells: Possible Role of Outer Membrane Proteins as Pathogenic Factors

    doi: 10.1128/IAI.69.8.5088-5097.2001

    Figure Lengend Snippet: (a) Enhanced expression of E-selectin and ICAM-1 in B. henselae- infected HUVEC. Bacteria were added to HUVEC monolayers in 96-well plates by centrifugation at 1,500 × g in a bacteria-to-cell ratio of 50:1. After 2 h plates were washed three times with fresh medium. After incubation for another 2 to 144 h, cells were processed for E-selectin or ICAM-1 cell surface ELISA. Note that E-selectin expression peaked at 7 to 12 h, while ICAM-1 increased up to 144 h. Data are means ± standard errors of the means of four separate experiments. (b) Northern blot showing increase of E-selectin and ICAM-1 mRNA in B. henselae- infected HUVEC. Total endothelial RNA was isolated, and levels of E-selectin-, ICAM-1, and GAPDH mRNA were quantitated. Note different time patterns of mRNA expression after B. henselae infection for E-selectin and ICAM-1 and the remarkably long upregulation of ICAM-1. A representative gel (of four independent experiments) is shown.

    Article Snippet: Purified freeze-dried monoclonal antibodies (MAbs) directed against E-selectin (1.2B6), vascular cell adhesion molecule 1 (VCAM-1) (1G11), and ICAM-1 (15.2) were from Dianova (Hamburg, Germany), and horseradish peroxidase-conjugated polyclonal sheep anti-mouse immunoglobulin G (IgG) antibodies (Abs) were from Amersham Pharmacia (Freiburg, Germany).

    Techniques: Expressing, Infection, Centrifugation, Incubation, Enzyme-linked Immunosorbent Assay, Northern Blot, Isolation

    (a) B. henselae- induced translocation of transcription factor NF-κB in HUVEC. An EMSA using a 32 P-labeled double-stranded NF-κB consensus oligonucleotide was performed. Nuclear proteins were extracted 10 to 180 min p.i. TNF-α was used as a positive control. Note biphasic NF-κB translocation in B. henselae- exposed HUVEC. Moreover, note the undiminished NF-κB signal in HUVEC treated with heat-inactivated polymyxin B (50 μg/ml)-exposed bacteria (right lane), suggesting that living bacteria and LPS are not central to NF-κB-translocation. A representative gel (of five independent experiments) is shown. (b) NF-κB upregulation was detected even at 72 h p.i. (c) Control experiments with a 2- to 20-fold molar excess of an NF-κB consensus oligonucleotide clearly demonstrate the specificity of the shift. (d) B. henselae- induced E-selectin and ICAM-1 expression was dose dependently reduced by NF-κB-specific inhibitor CAPE, as demonstrated by cell surface ELISA. Data are means ± standard errors of the means of three separate experiments.

    Journal: Infection and Immunity

    Article Title: Bartonella henselae Induces NF-?B-Dependent Upregulation of Adhesion Molecules in Cultured Human Endothelial Cells: Possible Role of Outer Membrane Proteins as Pathogenic Factors

    doi: 10.1128/IAI.69.8.5088-5097.2001

    Figure Lengend Snippet: (a) B. henselae- induced translocation of transcription factor NF-κB in HUVEC. An EMSA using a 32 P-labeled double-stranded NF-κB consensus oligonucleotide was performed. Nuclear proteins were extracted 10 to 180 min p.i. TNF-α was used as a positive control. Note biphasic NF-κB translocation in B. henselae- exposed HUVEC. Moreover, note the undiminished NF-κB signal in HUVEC treated with heat-inactivated polymyxin B (50 μg/ml)-exposed bacteria (right lane), suggesting that living bacteria and LPS are not central to NF-κB-translocation. A representative gel (of five independent experiments) is shown. (b) NF-κB upregulation was detected even at 72 h p.i. (c) Control experiments with a 2- to 20-fold molar excess of an NF-κB consensus oligonucleotide clearly demonstrate the specificity of the shift. (d) B. henselae- induced E-selectin and ICAM-1 expression was dose dependently reduced by NF-κB-specific inhibitor CAPE, as demonstrated by cell surface ELISA. Data are means ± standard errors of the means of three separate experiments.

    Article Snippet: Purified freeze-dried monoclonal antibodies (MAbs) directed against E-selectin (1.2B6), vascular cell adhesion molecule 1 (VCAM-1) (1G11), and ICAM-1 (15.2) were from Dianova (Hamburg, Germany), and horseradish peroxidase-conjugated polyclonal sheep anti-mouse immunoglobulin G (IgG) antibodies (Abs) were from Amersham Pharmacia (Freiburg, Germany).

    Techniques: Translocation Assay, Labeling, Positive Control, Expressing, Enzyme-linked Immunosorbent Assay

    (a) OMP-induced endothelial adhesion molecule expression was NF-κB dependent and unrelated to LPS. Effects of OMPs (500 ng/ml) on E-selectin and ICAM-1 expression were compared to those for untreated cells. When indicated, cells were pretreated with 5 or 25 μM CAPE 1 h before exposure to OMPs; this resulted in a dose-dependent reduction of adhesion molecule expression. When indicated, polymyxin B was added to OMPs or LPS in a concentration of 50 μg/ml. Data are means ± standard errors of the means of three separate experiments. (b) OMP induced translocation of transcription factor NF-κB in HUVEC. An EMSA was performed as described in Materials and Methods. Nuclear proteins were extracted 40 min p.i. TNF-α was used as a positive control. Note the weak NF-κB signal in LPS-exposed HUVEC compared to that for OMP-treated cells. A representative gel (from three independent experiments) is shown.

    Journal: Infection and Immunity

    Article Title: Bartonella henselae Induces NF-?B-Dependent Upregulation of Adhesion Molecules in Cultured Human Endothelial Cells: Possible Role of Outer Membrane Proteins as Pathogenic Factors

    doi: 10.1128/IAI.69.8.5088-5097.2001

    Figure Lengend Snippet: (a) OMP-induced endothelial adhesion molecule expression was NF-κB dependent and unrelated to LPS. Effects of OMPs (500 ng/ml) on E-selectin and ICAM-1 expression were compared to those for untreated cells. When indicated, cells were pretreated with 5 or 25 μM CAPE 1 h before exposure to OMPs; this resulted in a dose-dependent reduction of adhesion molecule expression. When indicated, polymyxin B was added to OMPs or LPS in a concentration of 50 μg/ml. Data are means ± standard errors of the means of three separate experiments. (b) OMP induced translocation of transcription factor NF-κB in HUVEC. An EMSA was performed as described in Materials and Methods. Nuclear proteins were extracted 40 min p.i. TNF-α was used as a positive control. Note the weak NF-κB signal in LPS-exposed HUVEC compared to that for OMP-treated cells. A representative gel (from three independent experiments) is shown.

    Article Snippet: Purified freeze-dried monoclonal antibodies (MAbs) directed against E-selectin (1.2B6), vascular cell adhesion molecule 1 (VCAM-1) (1G11), and ICAM-1 (15.2) were from Dianova (Hamburg, Germany), and horseradish peroxidase-conjugated polyclonal sheep anti-mouse immunoglobulin G (IgG) antibodies (Abs) were from Amersham Pharmacia (Freiburg, Germany).

    Techniques: Expressing, Concentration Assay, Translocation Assay, Positive Control

    (A) Western blot analysis of ICAM-1, GAPDH, p-p38 MAPK and total p38 MAPK in MSCs, EPCs and MSCs + EPCs, with or without IL-1β (25 µ g/ml) or p38 MAPK inhibitor SB203580 (20 µ mol/ml) treatment. Lanes 1–3, normally cultured MSCs, EPCs and MSCs + EPCs groups, respectively; lanes 4–6, IL-1β (25 µ g/ml)-stimulated MSCs, EPCs and MSCs + EPCs groups, respectively; lanes 7–9, p38 MAPK inhibitor SB203580 (20 µ mol/ml)-stimulated MSCs, EPCs and MSCs + EPCs groups, respectively. (B) ICAM-1/GAPDH and (C) p-p38 MAPK/total-p38 MAPK IOD relative values were determined. Data are presented as the means ± standard deviation of three independent experiments. * P

    Journal: International Journal of Molecular Medicine

    Article Title: Interleukin-1β induces intercellular adhesion molecule-1 expression, thus enhancing the adhesion between mesenchymal stem cells and endothelial progenitor cells via the p38 MAPK signaling pathway

    doi: 10.3892/ijmm.2018.3424

    Figure Lengend Snippet: (A) Western blot analysis of ICAM-1, GAPDH, p-p38 MAPK and total p38 MAPK in MSCs, EPCs and MSCs + EPCs, with or without IL-1β (25 µ g/ml) or p38 MAPK inhibitor SB203580 (20 µ mol/ml) treatment. Lanes 1–3, normally cultured MSCs, EPCs and MSCs + EPCs groups, respectively; lanes 4–6, IL-1β (25 µ g/ml)-stimulated MSCs, EPCs and MSCs + EPCs groups, respectively; lanes 7–9, p38 MAPK inhibitor SB203580 (20 µ mol/ml)-stimulated MSCs, EPCs and MSCs + EPCs groups, respectively. (B) ICAM-1/GAPDH and (C) p-p38 MAPK/total-p38 MAPK IOD relative values were determined. Data are presented as the means ± standard deviation of three independent experiments. * P

    Article Snippet: The membrane was blocked with 5% skim milk or 5% BSA, and incubated overnight with anti-ICAM-1 (ab171123, 1:500; Abcam), anti-p38 MAPK (cat. no. #8690; 1:1,000) and anti-p-p38 MAPK (cat. no. #4511; 1:1,000; both from Cell Signaling Technology, Inc., Danvers, MA, USA) at 4°C.

    Techniques: Western Blot, Cell Culture, Standard Deviation

    Adhesion of MSCs (DAPI, blue staining) and EPCs (Mitrotrack red, red staining) was detected in Matrigel-coated plates. (A) Adhesion of normally cultured MSCs and EPCs. Adhesion of MSCs and EPCs treated with (B) anti-ICAM-1 neutralizing antibody, (C) IL-1β (25 µ g/ml) and (D) p38 mitogen-activated protein kinase inhibitor SB203580 (20 µ mol/ml). (E–H) White-light image of (A–D), respectively. Scale bar, 100 µ m. EPCs, endothelial progenitor cells; ICAM-1, intercellular adhesion molecule-1; IL-1β, interleukin-1β; MSCs, mesenchymal stem cells.

    Journal: International Journal of Molecular Medicine

    Article Title: Interleukin-1β induces intercellular adhesion molecule-1 expression, thus enhancing the adhesion between mesenchymal stem cells and endothelial progenitor cells via the p38 MAPK signaling pathway

    doi: 10.3892/ijmm.2018.3424

    Figure Lengend Snippet: Adhesion of MSCs (DAPI, blue staining) and EPCs (Mitrotrack red, red staining) was detected in Matrigel-coated plates. (A) Adhesion of normally cultured MSCs and EPCs. Adhesion of MSCs and EPCs treated with (B) anti-ICAM-1 neutralizing antibody, (C) IL-1β (25 µ g/ml) and (D) p38 mitogen-activated protein kinase inhibitor SB203580 (20 µ mol/ml). (E–H) White-light image of (A–D), respectively. Scale bar, 100 µ m. EPCs, endothelial progenitor cells; ICAM-1, intercellular adhesion molecule-1; IL-1β, interleukin-1β; MSCs, mesenchymal stem cells.

    Article Snippet: The membrane was blocked with 5% skim milk or 5% BSA, and incubated overnight with anti-ICAM-1 (ab171123, 1:500; Abcam), anti-p38 MAPK (cat. no. #8690; 1:1,000) and anti-p-p38 MAPK (cat. no. #4511; 1:1,000; both from Cell Signaling Technology, Inc., Danvers, MA, USA) at 4°C.

    Techniques: Staining, Cell Culture

    Immunofluorescence detection of ICAM-1 expression. (A) (a–c) Expression of ICAM-1 (FITC) in MSCs, EPCs and MSCs + EPCs normally cultured in vitro, as determined by cell immunofluorescence under a laser confocal microscope. (d–f) Mouse IgG control (FITC) staining. (B) (a–c) Expression of ICAM-1 (FITC) in MSCs, EPCs and MSCs + EPCs treated with IL-1β (25 µ g/ml) in vitro . (d–f) Mouse IgG control (FITC) staining. (C) (a–c) Expression of ICAM-1 (FITC) in MSCs, EPCs and MSCs + EPCs treated with the p38 mitogen-activated protein kinase inhibitor SB203580 (20 µ mol/ml) in vitro . (d–f) Mouse IgG control (FITC) staining. Scale bar, 5 µ m. EPCs, endothelial progenitor cells; FITC, fluorescein isothiocyanate; ICAM-1, intercellular adhesion molecule-1; IgG, immunoglobulin G; IL-1β, interleukin-1β; MSCs, mesenchymal stem cells.

    Journal: International Journal of Molecular Medicine

    Article Title: Interleukin-1β induces intercellular adhesion molecule-1 expression, thus enhancing the adhesion between mesenchymal stem cells and endothelial progenitor cells via the p38 MAPK signaling pathway

    doi: 10.3892/ijmm.2018.3424

    Figure Lengend Snippet: Immunofluorescence detection of ICAM-1 expression. (A) (a–c) Expression of ICAM-1 (FITC) in MSCs, EPCs and MSCs + EPCs normally cultured in vitro, as determined by cell immunofluorescence under a laser confocal microscope. (d–f) Mouse IgG control (FITC) staining. (B) (a–c) Expression of ICAM-1 (FITC) in MSCs, EPCs and MSCs + EPCs treated with IL-1β (25 µ g/ml) in vitro . (d–f) Mouse IgG control (FITC) staining. (C) (a–c) Expression of ICAM-1 (FITC) in MSCs, EPCs and MSCs + EPCs treated with the p38 mitogen-activated protein kinase inhibitor SB203580 (20 µ mol/ml) in vitro . (d–f) Mouse IgG control (FITC) staining. Scale bar, 5 µ m. EPCs, endothelial progenitor cells; FITC, fluorescein isothiocyanate; ICAM-1, intercellular adhesion molecule-1; IgG, immunoglobulin G; IL-1β, interleukin-1β; MSCs, mesenchymal stem cells.

    Article Snippet: The membrane was blocked with 5% skim milk or 5% BSA, and incubated overnight with anti-ICAM-1 (ab171123, 1:500; Abcam), anti-p38 MAPK (cat. no. #8690; 1:1,000) and anti-p-p38 MAPK (cat. no. #4511; 1:1,000; both from Cell Signaling Technology, Inc., Danvers, MA, USA) at 4°C.

    Techniques: Immunofluorescence, Expressing, Cell Culture, In Vitro, Microscopy, Staining

    2′- O -methyl modification of the 736 sense strand eliminates TNFR1 knockdown. ( A ) Hybrid 736 siRNA duplexes were prepared by annealing unmodified 736 RNA oligos (sense or antisense) with complementary RNA oligos modified by 2′- O -methylation, (such hybrid duplexes are indicated as 736/S or 736/AS). Dual modified duplexes (736/S+AS) and wild-type 736 (736/WT) were also prepared. 2′- O -Me modified bases are in bold and underlined. ( B ) HUVEC were mock-transfected or transfected with 10 nM LFA-3, an irrelevant siRNA, 736/WT, 736/S, 736/AS or 736/S + AS siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for ICAM-1 and E-selectin and analyzed by flow cytometry. Corrected MFIs were converted to ‘% Remaining’ relative to mock expression. ( C ) Hybrid siRNA-transfected HUVEC lysates were analyzed by western blot for the expression of TNFR1 and β-actin. Representative of one of two experiments with similar results.

    Journal: Nucleic Acids Research

    Article Title: Knockdown of TNFR1 by the sense strand of an ICAM-1 siRNA: dissection of an off-target effect

    doi: 10.1093/nar/gkm630

    Figure Lengend Snippet: 2′- O -methyl modification of the 736 sense strand eliminates TNFR1 knockdown. ( A ) Hybrid 736 siRNA duplexes were prepared by annealing unmodified 736 RNA oligos (sense or antisense) with complementary RNA oligos modified by 2′- O -methylation, (such hybrid duplexes are indicated as 736/S or 736/AS). Dual modified duplexes (736/S+AS) and wild-type 736 (736/WT) were also prepared. 2′- O -Me modified bases are in bold and underlined. ( B ) HUVEC were mock-transfected or transfected with 10 nM LFA-3, an irrelevant siRNA, 736/WT, 736/S, 736/AS or 736/S + AS siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for ICAM-1 and E-selectin and analyzed by flow cytometry. Corrected MFIs were converted to ‘% Remaining’ relative to mock expression. ( C ) Hybrid siRNA-transfected HUVEC lysates were analyzed by western blot for the expression of TNFR1 and β-actin. Representative of one of two experiments with similar results.

    Article Snippet: FACS analysis siRNA-transfected HUVEC expression of ICAM-1, E-selectin, VCAM-1 and MHC class I were determined by FACS analysis (FACSort, Becton Dickinson) after immunostaining with saturating concentrations of directly labeled antigen-specific or isotype-matched monoclonal antibodies.

    Techniques: Modification, Methylation, Transfection, Staining, Flow Cytometry, Cytometry, Expressing, Western Blot

    736 Inhibits TNF-mediated HUVEC antigen expression. HUVEC were mock-transfected or transfected with 10 nM 736 or lamin siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for E-selectin, ICAM-1, VCAM-1 and MHC I and analyzed by flow cytometry. Filled histograms represent antigen-specific staining and empty histograms represent isotype control staining. Corrected MFI in the upper right hand corner = antigen-specific MFI minus isotype MFI. Representative of one of three experiments with similar results.

    Journal: Nucleic Acids Research

    Article Title: Knockdown of TNFR1 by the sense strand of an ICAM-1 siRNA: dissection of an off-target effect

    doi: 10.1093/nar/gkm630

    Figure Lengend Snippet: 736 Inhibits TNF-mediated HUVEC antigen expression. HUVEC were mock-transfected or transfected with 10 nM 736 or lamin siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for E-selectin, ICAM-1, VCAM-1 and MHC I and analyzed by flow cytometry. Filled histograms represent antigen-specific staining and empty histograms represent isotype control staining. Corrected MFI in the upper right hand corner = antigen-specific MFI minus isotype MFI. Representative of one of three experiments with similar results.

    Article Snippet: FACS analysis siRNA-transfected HUVEC expression of ICAM-1, E-selectin, VCAM-1 and MHC class I were determined by FACS analysis (FACSort, Becton Dickinson) after immunostaining with saturating concentrations of directly labeled antigen-specific or isotype-matched monoclonal antibodies.

    Techniques: Expressing, Transfection, Staining, Flow Cytometry, Cytometry

    736 siRNA selectively targets TNFR1 mRNA and protein and selectively inhibits TNF responses. ( A ) HUVEC were mock-transfected or transfected with 736 or lamin siRNA. Cell lysates were prepared 24 h after the last transfection, resolved by SDS-PAGE, and immunoblotted with antibodies specific for TNF receptor signaling proteins. ( B ) HUVEC were transfected with 736 or lamin siRNA. cDNA from each culture was analyzed by qRT-PCR using TNF signalosome-specific primers. Values were normalized using actin controls and converted to ‘% mRNA Remaining’ relative to mock expression levels. Representative of one of two experiments with similar results. ( C ) HUVEC were transfected with 736 or lamin siRNA. Cells were then stimulated for 24 h with either TNF (10 ng/ml) or IL-1β (50 ng/ml), immuno-stained using fluorescent antigen-specific antibody for ICAM-1 and analyzed by flow cytometry.

    Journal: Nucleic Acids Research

    Article Title: Knockdown of TNFR1 by the sense strand of an ICAM-1 siRNA: dissection of an off-target effect

    doi: 10.1093/nar/gkm630

    Figure Lengend Snippet: 736 siRNA selectively targets TNFR1 mRNA and protein and selectively inhibits TNF responses. ( A ) HUVEC were mock-transfected or transfected with 736 or lamin siRNA. Cell lysates were prepared 24 h after the last transfection, resolved by SDS-PAGE, and immunoblotted with antibodies specific for TNF receptor signaling proteins. ( B ) HUVEC were transfected with 736 or lamin siRNA. cDNA from each culture was analyzed by qRT-PCR using TNF signalosome-specific primers. Values were normalized using actin controls and converted to ‘% mRNA Remaining’ relative to mock expression levels. Representative of one of two experiments with similar results. ( C ) HUVEC were transfected with 736 or lamin siRNA. Cells were then stimulated for 24 h with either TNF (10 ng/ml) or IL-1β (50 ng/ml), immuno-stained using fluorescent antigen-specific antibody for ICAM-1 and analyzed by flow cytometry.

    Article Snippet: FACS analysis siRNA-transfected HUVEC expression of ICAM-1, E-selectin, VCAM-1 and MHC class I were determined by FACS analysis (FACSort, Becton Dickinson) after immunostaining with saturating concentrations of directly labeled antigen-specific or isotype-matched monoclonal antibodies.

    Techniques: Transfection, SDS Page, Quantitative RT-PCR, Expressing, Staining, Flow Cytometry, Cytometry

    5′ phosphorylation of the 736 sense strand is required for effective TNFR1 knockdown. Hybrid 736 siRNA duplexes were prepared by annealing wild-type 736 antisense RNA oligos with either wild-type 736 sense strand oligos [736 (WT)] or 5′deoxy capped 736 sense strand oligos [736 (5′Cap)]. HUVEC were mock-transfected or transfected with 10 nM lamin, 736 (WT), or 736 (5′Cap) siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for E-selectin and ICAM-1 and analyzed by flow cytometry. Filled histograms represent antigen-specific staining and empty histograms represent isotype control staining. Corrected MFI in the upper right hand corner = antigen-specific MFI minus isotype MFI. Representative of one of two experiments with similar results.

    Journal: Nucleic Acids Research

    Article Title: Knockdown of TNFR1 by the sense strand of an ICAM-1 siRNA: dissection of an off-target effect

    doi: 10.1093/nar/gkm630

    Figure Lengend Snippet: 5′ phosphorylation of the 736 sense strand is required for effective TNFR1 knockdown. Hybrid 736 siRNA duplexes were prepared by annealing wild-type 736 antisense RNA oligos with either wild-type 736 sense strand oligos [736 (WT)] or 5′deoxy capped 736 sense strand oligos [736 (5′Cap)]. HUVEC were mock-transfected or transfected with 10 nM lamin, 736 (WT), or 736 (5′Cap) siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for E-selectin and ICAM-1 and analyzed by flow cytometry. Filled histograms represent antigen-specific staining and empty histograms represent isotype control staining. Corrected MFI in the upper right hand corner = antigen-specific MFI minus isotype MFI. Representative of one of two experiments with similar results.

    Article Snippet: FACS analysis siRNA-transfected HUVEC expression of ICAM-1, E-selectin, VCAM-1 and MHC class I were determined by FACS analysis (FACSort, Becton Dickinson) after immunostaining with saturating concentrations of directly labeled antigen-specific or isotype-matched monoclonal antibodies.

    Techniques: Transfection, Staining, Flow Cytometry, Cytometry

    Complementarity between TNFR1 and ICAM-1 does not activate a natural antisense transcript (NAT) activity. ( A ) HUVEC cell lines expressing EGFP/TNFR1 3′UTR chimeric constructs were treated for 24 h with increasing concentrations of TNF to induce ICAM-1 expression. ICAM-1 expression levels were determined by FACS using an ICAM-1-specific antibody. ( B ) HDMEC cell lines overexpressing E-selectin and ICAM-1 were tested to determine basal TNFR1 cell surface levels. Cells were immunostained with fluorescently labeled antibody specific for ICAM-1, TNFR1 and TNFR2 then analyzed by FACS. Representative of one of two independent experiments with similar results.

    Journal: Nucleic Acids Research

    Article Title: Knockdown of TNFR1 by the sense strand of an ICAM-1 siRNA: dissection of an off-target effect

    doi: 10.1093/nar/gkm630

    Figure Lengend Snippet: Complementarity between TNFR1 and ICAM-1 does not activate a natural antisense transcript (NAT) activity. ( A ) HUVEC cell lines expressing EGFP/TNFR1 3′UTR chimeric constructs were treated for 24 h with increasing concentrations of TNF to induce ICAM-1 expression. ICAM-1 expression levels were determined by FACS using an ICAM-1-specific antibody. ( B ) HDMEC cell lines overexpressing E-selectin and ICAM-1 were tested to determine basal TNFR1 cell surface levels. Cells were immunostained with fluorescently labeled antibody specific for ICAM-1, TNFR1 and TNFR2 then analyzed by FACS. Representative of one of two independent experiments with similar results.

    Article Snippet: FACS analysis siRNA-transfected HUVEC expression of ICAM-1, E-selectin, VCAM-1 and MHC class I were determined by FACS analysis (FACSort, Becton Dickinson) after immunostaining with saturating concentrations of directly labeled antigen-specific or isotype-matched monoclonal antibodies.

    Techniques: Activity Assay, Expressing, Construct, FACS, Labeling

    Cell surface expression of LFA-1 and ICAM-1 on Jurkat cells. FACS analysis of expression of CD18 (beta subunit of LFA-1) and ICAM-1 on Jurkat cells expressing ITK (no shRNA, n.t. shRNA) or not expressing ITK (258 shRNA, 614 shRNA) by using anti-CD18-FITC antibody and anti-ICAM-FITC. Filled histograms represent the isotype control. All figures show one representative experiment out of three repetitions.

    Journal: Scientific Reports

    Article Title: IL-2 Inducible Kinase ITK is Critical for HIV-1 Infection of Jurkat T-cells

    doi: 10.1038/s41598-018-21344-7

    Figure Lengend Snippet: Cell surface expression of LFA-1 and ICAM-1 on Jurkat cells. FACS analysis of expression of CD18 (beta subunit of LFA-1) and ICAM-1 on Jurkat cells expressing ITK (no shRNA, n.t. shRNA) or not expressing ITK (258 shRNA, 614 shRNA) by using anti-CD18-FITC antibody and anti-ICAM-FITC. Filled histograms represent the isotype control. All figures show one representative experiment out of three repetitions.

    Article Snippet: LFA-1 was stained with 2 µl FITC-labeled anti-CD18 antibody (Beckman Coulter) and ICAM-1 with 2 µl anti-ICAM-1 (CD54) clone HA58 FITC (eBioscience, San Diego, USA), both for 30 min at room temperature.

    Techniques: Expressing, FACS, shRNA

    Regulation of ICAM1 through ALK stimulation. ICAM1 expression in nasal biopsies from patients with CRSwNP and healthy controls (n = 6–7) ( a ). ICAM1 expression on cultured epithelial cells (n = 5) ( b ) or stimulated with TGF-β1 ( c ), Activin A ( d ), BMP4 ( e ) or Activin B ( f ) for 24 h (n = 3). White bars (Control epithelial cells), gray bars (Polyp epithelial cells). Values: mean ± SEM. Friedman-test with Dunn’s post-test, was used for comparisons of more than two data sets. An unpaired t- test was used to compare two sets of data.

    Journal: Scientific Reports

    Article Title: Activation of Activin receptor-like kinases curbs mucosal inflammation and proliferation in chronic rhinosinusitis with nasal polyps

    doi: 10.1038/s41598-018-19955-1

    Figure Lengend Snippet: Regulation of ICAM1 through ALK stimulation. ICAM1 expression in nasal biopsies from patients with CRSwNP and healthy controls (n = 6–7) ( a ). ICAM1 expression on cultured epithelial cells (n = 5) ( b ) or stimulated with TGF-β1 ( c ), Activin A ( d ), BMP4 ( e ) or Activin B ( f ) for 24 h (n = 3). White bars (Control epithelial cells), gray bars (Polyp epithelial cells). Values: mean ± SEM. Friedman-test with Dunn’s post-test, was used for comparisons of more than two data sets. An unpaired t- test was used to compare two sets of data.

    Article Snippet: Sections were either incubated with primary mouse anti-human antibodies against IL-8 (1:1000, ab18672), rabbit anti-human antibodies against Ki67 (1:5000, ab15580) or ICAM1 (1:100, ab109361, all from Abcam) overnight and subsequently incubated for 1 h with a secondary goat anti-mouse antibody (1:200, Vector Laboratories, Peterborough, United Kingdom) or goat anti-rabbit antibody (1:200, Vector Laboratories).

    Techniques: Expressing, Cell Culture

    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 Downregulated the mRNA Expression of MCP-1, ICAM-1, and TNF-α in Rats with Ischemic AKI Compared with sham-operated rats, the mRNA expression of inflammatory mediators, MCP-1, ICAM-1, and TNF-α , increased significantly at 12 h of reperfusion in rats with ischemic AKI, while pretreatment with AS-IV apparently downregulated the mRNA expression of TNF-α , MCP-1 , and ICAM-1 ( ) in rats with ischemic AKI at the same time point.

    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 Downregulated the mRNA Expression of MCP-1, ICAM-1, and TNF-α in Rats with Ischemic AKI Compared with sham-operated rats, the mRNA expression of inflammatory mediators, MCP-1, ICAM-1, and TNF-α , increased significantly at 12 h of reperfusion in rats with ischemic AKI, while pretreatment with AS-IV apparently downregulated the mRNA expression of TNF-α , MCP-1 , and ICAM-1 ( ) in rats with ischemic AKI at the same time point.

    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 Downregulated the mRNA Expression of MCP-1, ICAM-1, and TNF-α in Rats with Ischemic AKI Compared with sham-operated rats, the mRNA expression of inflammatory mediators, MCP-1, ICAM-1, and TNF-α , increased significantly at 12 h of reperfusion in rats with ischemic AKI, while pretreatment with AS-IV apparently downregulated the mRNA expression of TNF-α , MCP-1 , and ICAM-1 ( ) in rats with ischemic AKI at the same time point.

    Techniques:

    RelB overexpression reduces cigarette smoke–induced ICAM-1 expression in mouse lungs. Mice were treated with either the RelB or control virus (two doses of 5 × 10 8 plaque-forming units per mouse delivered 24 hours apart) and exposed to

    Journal: The American Journal of Pathology

    Article Title: Lung-Targeted Overexpression of the NF-?B Member RelB Inhibits Cigarette Smoke-Induced Inflammation

    doi: 10.1016/j.ajpath.2011.03.030

    Figure Lengend Snippet: RelB overexpression reduces cigarette smoke–induced ICAM-1 expression in mouse lungs. Mice were treated with either the RelB or control virus (two doses of 5 × 10 8 plaque-forming units per mouse delivered 24 hours apart) and exposed to

    Article Snippet: ICAM-1 was targeted with an ICAM-1–specific antibody (AF796; R & D Systems) and detected with a Texas Red–conjugated secondary antibody.

    Techniques: Over Expression, Expressing, Mouse Assay

    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:

    R1R2 decreases TNF-α-induced monocyte U937 cell adhesion to HUVECs and transendothelial migration and reduces ICAM-1 and VCAM-1 levels. (A) HUVECs were pretreated with R1R2 or scramble peptide before treatment with TNF-α (10ng/ml) for 6 hours in the continued presence of R1R2 or scrambled peptide. Calcein-AM labeled U937 monocyte adhesion to TNF-α HUVECs was quantitated by fluorescence intensity. Microscopic images showing U937 monocytes adhering to HUVECs as assessed by in vitro adhesion assay. (B) Calcein-AM-labeled U937 monocytes transmigrated through TNF-α-treated HUVECs. (C) Western blot analysis of ICAM-1 and VCAM-1 expression in TNF-α-treated HUVECs. * indicates p

    Journal: PLoS ONE

    Article Title: Collagen Inhibitory Peptide R1R2 Mediates Vascular Remodeling by Decreasing Inflammation and Smooth Muscle Cell Activation

    doi: 10.1371/journal.pone.0117356

    Figure Lengend Snippet: R1R2 decreases TNF-α-induced monocyte U937 cell adhesion to HUVECs and transendothelial migration and reduces ICAM-1 and VCAM-1 levels. (A) HUVECs were pretreated with R1R2 or scramble peptide before treatment with TNF-α (10ng/ml) for 6 hours in the continued presence of R1R2 or scrambled peptide. Calcein-AM labeled U937 monocyte adhesion to TNF-α HUVECs was quantitated by fluorescence intensity. Microscopic images showing U937 monocytes adhering to HUVECs as assessed by in vitro adhesion assay. (B) Calcein-AM-labeled U937 monocytes transmigrated through TNF-α-treated HUVECs. (C) Western blot analysis of ICAM-1 and VCAM-1 expression in TNF-α-treated HUVECs. * indicates p

    Article Snippet: The membranes were incubated with antibody to collagen type I (1:1000; Millipore, Billerica, MA), FN (1:8000; Sigma-Aldrich, St. Louis, MO), ICAM-1 (1:500; GeneTex, Irvine, CA), VCAM-1 (1:1000; Santa Cruz Biotechnology, Dallas, Texas), or GAPDH (1:5000, Sigma-Aldrich, St. Louis, MO) overnight, followed by horseradish peroxidase–conjugated secondary antibodies (1:12000; BioRad, Hercules, CA) for 1 h at room temperature.

    Techniques: Migration, Labeling, Fluorescence, In Vitro, Cell Adhesion Assay, Western Blot, Expressing

    R1R2 decreases inflammatory cell accumulation and VCAM-1 and ICAM-1 levels. (A) Photographs showing representative immunostaining of CD-45, VCAM-1 and ICAM-1 in the left carotid artery from the animals subjected to ligation 7 days after the surgery. Arrows indicate CD45 (+) leukocytes. Bar, 50 μm. (B-D) Percentage of the area which is CD45 (+) (Sham: n = 7, Scrambled: n = 6, R1R2: n = 5) (B), VCAM-1 (+) (Sham: n = 7, Scrambled: n = 9, R1R2: n = 7) (C) or ICAM-1 (+) (Sham: n = 5, Scrambled: n = 8, R1R2: n = 7) (D) were assessed in the intima-media of the vessel. (E) Western blot analysis of ICAM-1 and VCAM-1 expression in ligated carotid artery at 7 days. Equal protein loading was confirmed with GAPDH. * indicates p

    Journal: PLoS ONE

    Article Title: Collagen Inhibitory Peptide R1R2 Mediates Vascular Remodeling by Decreasing Inflammation and Smooth Muscle Cell Activation

    doi: 10.1371/journal.pone.0117356

    Figure Lengend Snippet: R1R2 decreases inflammatory cell accumulation and VCAM-1 and ICAM-1 levels. (A) Photographs showing representative immunostaining of CD-45, VCAM-1 and ICAM-1 in the left carotid artery from the animals subjected to ligation 7 days after the surgery. Arrows indicate CD45 (+) leukocytes. Bar, 50 μm. (B-D) Percentage of the area which is CD45 (+) (Sham: n = 7, Scrambled: n = 6, R1R2: n = 5) (B), VCAM-1 (+) (Sham: n = 7, Scrambled: n = 9, R1R2: n = 7) (C) or ICAM-1 (+) (Sham: n = 5, Scrambled: n = 8, R1R2: n = 7) (D) were assessed in the intima-media of the vessel. (E) Western blot analysis of ICAM-1 and VCAM-1 expression in ligated carotid artery at 7 days. Equal protein loading was confirmed with GAPDH. * indicates p

    Article Snippet: The membranes were incubated with antibody to collagen type I (1:1000; Millipore, Billerica, MA), FN (1:8000; Sigma-Aldrich, St. Louis, MO), ICAM-1 (1:500; GeneTex, Irvine, CA), VCAM-1 (1:1000; Santa Cruz Biotechnology, Dallas, Texas), or GAPDH (1:5000, Sigma-Aldrich, St. Louis, MO) overnight, followed by horseradish peroxidase–conjugated secondary antibodies (1:12000; BioRad, Hercules, CA) for 1 h at room temperature.

    Techniques: Immunostaining, Ligation, Western Blot, Expressing

    Affinity and antigen-density dependent activation of Jurkat CAR T cells in vitro . ( a ) Top, histograms depicting 8 μm latex beads coupled with known amounts of R6.5 antibody conjugated with cy5.5 (10 3 –10 7 antibodies per bead). The level of shift after incubation with R6.5 (black) from non-labeled (grey) was used to estimate ICAM-1 density in each indicated target cell line. 8505 C/-ICAM-1; 8505 C cells with ICAM-1 gene inactivation by CRISPR/Cas9. 8505 C/LPS, 8505 C cells were incubated with LPS to induce overexpression of ICAM-1. ( b ) CD25 expression in Jurkat CAR T cells (WT, F292A, F292G, and TM) after co-incubation with different target cell lines for 24 h (n = 3–4). p

    Journal: Scientific Reports

    Article Title: Micromolar affinity CAR T cells to ICAM-1 achieves rapid tumor elimination while avoiding systemic toxicity

    doi: 10.1038/s41598-017-14749-3

    Figure Lengend Snippet: Affinity and antigen-density dependent activation of Jurkat CAR T cells in vitro . ( a ) Top, histograms depicting 8 μm latex beads coupled with known amounts of R6.5 antibody conjugated with cy5.5 (10 3 –10 7 antibodies per bead). The level of shift after incubation with R6.5 (black) from non-labeled (grey) was used to estimate ICAM-1 density in each indicated target cell line. 8505 C/-ICAM-1; 8505 C cells with ICAM-1 gene inactivation by CRISPR/Cas9. 8505 C/LPS, 8505 C cells were incubated with LPS to induce overexpression of ICAM-1. ( b ) CD25 expression in Jurkat CAR T cells (WT, F292A, F292G, and TM) after co-incubation with different target cell lines for 24 h (n = 3–4). p

    Article Snippet: I domain Jurkat T cell variants were incubated with 10 µg/ml recombinant human ICAM-1 fused to human Fcγ (R & D Systems).

    Techniques: Activation Assay, In Vitro, Incubation, Labeling, CRISPR, Over Expression, Expressing

    Analysis of systemic toxicity by flow cytometry and histology. ( a ) Flow cytometry analysis of total cells harvested from the lungs of non treated (No T) or treated (TM CAR) mice. GFP and CD3 were used as markers of 8505 C tumor and T cells, respectively. Mice treated with TM CAR T cells were sacrificed at different time points to represent the association between tumor burden and TM CAR T cells. ( b ) Lung tissues harvested from untreated mice and mice treated with TM and F292A CAR T cells were processed for H E, GFP and CD3 staining. The scale bar in each image is 2 mm. Tissue sacrifice time points are indicated on the left. For example, X20T10 represents 20 days post tumor x enograft and 10 days post T cell infusion. ( c ) Murine ICAM-1 expression in lung cells harvested from tumor-bearing mice after treatment with TM CAR T cells.

    Journal: Scientific Reports

    Article Title: Micromolar affinity CAR T cells to ICAM-1 achieves rapid tumor elimination while avoiding systemic toxicity

    doi: 10.1038/s41598-017-14749-3

    Figure Lengend Snippet: Analysis of systemic toxicity by flow cytometry and histology. ( a ) Flow cytometry analysis of total cells harvested from the lungs of non treated (No T) or treated (TM CAR) mice. GFP and CD3 were used as markers of 8505 C tumor and T cells, respectively. Mice treated with TM CAR T cells were sacrificed at different time points to represent the association between tumor burden and TM CAR T cells. ( b ) Lung tissues harvested from untreated mice and mice treated with TM and F292A CAR T cells were processed for H E, GFP and CD3 staining. The scale bar in each image is 2 mm. Tissue sacrifice time points are indicated on the left. For example, X20T10 represents 20 days post tumor x enograft and 10 days post T cell infusion. ( c ) Murine ICAM-1 expression in lung cells harvested from tumor-bearing mice after treatment with TM CAR T cells.

    Article Snippet: I domain Jurkat T cell variants were incubated with 10 µg/ml recombinant human ICAM-1 fused to human Fcγ (R & D Systems).

    Techniques: Flow Cytometry, Cytometry, Mouse Assay, Staining, Expressing

    Construction of ICAM-1 specific CARs with step-wise, 10 6 -fold variations in affinity. ( a ) Schematic of LFA-1 in complex with ICAM-1. α and β chains, and modular domains of LFA-1 integrin are labeled. I domain of α chain is denoted with a dotted box. Metal ions necessary for LFA-1 and ICAM-1 interaction are shown in circles. ( b ) Structural model of LFA-1 I domain and the N-terminal domain of ICAM-1 (D1) are drawn in ribbon diagram. N and C-termini, and mutational hot spots are indicated. ( c ) SPR sensogram of I domain variants binding to immobilized human ICAM-1, except F265S/F292G*, which was flowed over murine ICAM-1 (adapted from Fig. 2 of Jin et al . 27 , and Fig. 1 of Wong et al . 28 ). ( d ) A schematic of the lentivirus vector encoding I domain CAR. LTR = long terminal repeat; SD = splice donor; SA = splice acceptor; ψ + = packaging signal; SS = signal sequence; TM = transmembrane; Cyt = cytosolic domain. ( e ) Anti-Myc antibody binding to Jurkat T cells transduced with Myc-tagged CARs (TM, F292G, F292A, and WT I domain). NT = non-transduced. ( f ) Recombinant ICAM-1-Fc binding to CARs expressed in HEK 293 T cells. ( g ) V-bottom adhesion assay measuring relative binding affinities between I domain CARs expressed in Jurkat T cells and soluble human (top) and murine (bottom) ICAM-1 (CD54) coated surfaces. n = 3; p

    Journal: Scientific Reports

    Article Title: Micromolar affinity CAR T cells to ICAM-1 achieves rapid tumor elimination while avoiding systemic toxicity

    doi: 10.1038/s41598-017-14749-3

    Figure Lengend Snippet: Construction of ICAM-1 specific CARs with step-wise, 10 6 -fold variations in affinity. ( a ) Schematic of LFA-1 in complex with ICAM-1. α and β chains, and modular domains of LFA-1 integrin are labeled. I domain of α chain is denoted with a dotted box. Metal ions necessary for LFA-1 and ICAM-1 interaction are shown in circles. ( b ) Structural model of LFA-1 I domain and the N-terminal domain of ICAM-1 (D1) are drawn in ribbon diagram. N and C-termini, and mutational hot spots are indicated. ( c ) SPR sensogram of I domain variants binding to immobilized human ICAM-1, except F265S/F292G*, which was flowed over murine ICAM-1 (adapted from Fig. 2 of Jin et al . 27 , and Fig. 1 of Wong et al . 28 ). ( d ) A schematic of the lentivirus vector encoding I domain CAR. LTR = long terminal repeat; SD = splice donor; SA = splice acceptor; ψ + = packaging signal; SS = signal sequence; TM = transmembrane; Cyt = cytosolic domain. ( e ) Anti-Myc antibody binding to Jurkat T cells transduced with Myc-tagged CARs (TM, F292G, F292A, and WT I domain). NT = non-transduced. ( f ) Recombinant ICAM-1-Fc binding to CARs expressed in HEK 293 T cells. ( g ) V-bottom adhesion assay measuring relative binding affinities between I domain CARs expressed in Jurkat T cells and soluble human (top) and murine (bottom) ICAM-1 (CD54) coated surfaces. n = 3; p

    Article Snippet: I domain Jurkat T cell variants were incubated with 10 µg/ml recombinant human ICAM-1 fused to human Fcγ (R & D Systems).

    Techniques: Labeling, SPR Assay, Binding Assay, Plasmid Preparation, Sequencing, Transduction, Recombinant, Cell Adhesion Assay

    Representative immunohistochemical staining against ETR in skin equivalents topically treated with ETR dissolved in PBS (a) or encapsulated in tNG_pNIPAM (b) or tNG_tPG (c). Images show pseudo coloured ETR temperature staining (scale and direction of increasing signal intensity shown on the right) overlaid onto differential interference contrast (DIC) images, onto which the boundaries between the stratum corneum / viable epidermis (upper) and the viable epidermis / dermis (lower) have been marked (scale bar = 50 µm). Protein levels of TNFα, TSLP and ICAM1 in TNFα treated skin equivalents (black) calculated as a percentage of normal skin equivalents (grey) (d). Protein levels of TNFα (e), TSLP (f) and ICAM1 (g) in TNFα treated skin equivalents following treatment with empty (grey) or ETR loaded (black) tNGs or PBS. Values are expressed as a percentage of TNFα treated controls. Insets show representative western blots from the protein of interest, above, and β actin, below. Dashed lines indicate mean protein levels found in untreated, normal skin equivalents. Statistical differences from the normal controls (d) or TNFα treated controls (e-f) were calculated by Student's t -test (n = 3, error bars = SEM, * = p ≤ 0.05).

    Journal: Theranostics

    Article Title: Breaking the Barrier - Potent Anti-Inflammatory Activity following Efficient Topical Delivery of Etanercept using Thermoresponsive Nanogels

    doi: 10.7150/thno.21668

    Figure Lengend Snippet: Representative immunohistochemical staining against ETR in skin equivalents topically treated with ETR dissolved in PBS (a) or encapsulated in tNG_pNIPAM (b) or tNG_tPG (c). Images show pseudo coloured ETR temperature staining (scale and direction of increasing signal intensity shown on the right) overlaid onto differential interference contrast (DIC) images, onto which the boundaries between the stratum corneum / viable epidermis (upper) and the viable epidermis / dermis (lower) have been marked (scale bar = 50 µm). Protein levels of TNFα, TSLP and ICAM1 in TNFα treated skin equivalents (black) calculated as a percentage of normal skin equivalents (grey) (d). Protein levels of TNFα (e), TSLP (f) and ICAM1 (g) in TNFα treated skin equivalents following treatment with empty (grey) or ETR loaded (black) tNGs or PBS. Values are expressed as a percentage of TNFα treated controls. Insets show representative western blots from the protein of interest, above, and β actin, below. Dashed lines indicate mean protein levels found in untreated, normal skin equivalents. Statistical differences from the normal controls (d) or TNFα treated controls (e-f) were calculated by Student's t -test (n = 3, error bars = SEM, * = p ≤ 0.05).

    Article Snippet: For primary antibodies, anti-TNFα (ab183896), anti-TSLP (ab47943), and anti-ICAM1 (ab53013) were purchased from abcam (Cambridge, UK).

    Techniques: Immunohistochemistry, Staining, Western Blot

    Del-1 inhibits ICAM-1-dependent chemokine production by neutrophils. (a)–(c) ATRA-differentiated HL-60 neutrophils were cultured for 24 hours on plates coated with Fc protein control, ICAM-1-Fc, or Del-1-Fc, and induction of release of CCL3 (a), CXCL2 (b), and TNF (c) was assayed by ELISA. (d)-(e) ATRA-differentiated HL-60 neutrophils were cultured for 24 hours on ICAM-1-Fc-coated plates in the presence of the indicated concentrations of soluble Del-1, and induction of release of CCL3 (d) and CXCL2 (e) was assayed by ELISA. (f)-(g) ATRA-differentiated HL-60 neutrophils were stimulated for 24 hours with 1 μ g/mL Pam 3 CSK 4 or 0.1 μ g/mL LPS, in the absence or presence of the indicated concentrations of Del-1, and induction of release of CCL3 (f) and CXCL2 (g) was assayed by ELISA. Data are means ± SD ((a)–(e), n ≥ 4 and (f)-(g), n = 2 sets of HL-60 cells). * P

    Journal: Clinical and Developmental Immunology

    Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue

    doi: 10.1155/2013/617809

    Figure Lengend Snippet: Del-1 inhibits ICAM-1-dependent chemokine production by neutrophils. (a)–(c) ATRA-differentiated HL-60 neutrophils were cultured for 24 hours on plates coated with Fc protein control, ICAM-1-Fc, or Del-1-Fc, and induction of release of CCL3 (a), CXCL2 (b), and TNF (c) was assayed by ELISA. (d)-(e) ATRA-differentiated HL-60 neutrophils were cultured for 24 hours on ICAM-1-Fc-coated plates in the presence of the indicated concentrations of soluble Del-1, and induction of release of CCL3 (d) and CXCL2 (e) was assayed by ELISA. (f)-(g) ATRA-differentiated HL-60 neutrophils were stimulated for 24 hours with 1 μ g/mL Pam 3 CSK 4 or 0.1 μ g/mL LPS, in the absence or presence of the indicated concentrations of Del-1, and induction of release of CCL3 (f) and CXCL2 (g) was assayed by ELISA. Data are means ± SD ((a)–(e), n ≥ 4 and (f)-(g), n = 2 sets of HL-60 cells). * P

    Article Snippet: In new experiments in WT mice, we monitored the periodontal expression of Del-1 in parallel with ICAM-1, VCAM-1, and E-selectin from the age of 5 weeks to very old age (up to 24 months) ( ).

    Techniques: Cell Culture, Enzyme-linked Immunosorbent Assay

    Regulation of Del-1 versus ICAM-1 and VCAM-1 by inflammatory stimuli. HUVEC were cultured for the indicated time intervals with 10 ng/mL TNF (a), 5 μ g/mL serum amyloid A (SAA; (b)), P. gingivalis (Pg; MOI = 10 : 1) (c), Pam 3 CSK 4 or LPS (both at 0.5 μ g/mL; (d)), 10 ng/mL IFN γ (e), or IL-17A or IL-17F (both at 10 ng/mL; (f)) and assayed for Del-1, ICAM-1, and VCAM-1 mRNA expression. Results were normalized to those of GAPDH mRNA and expressed as fold change in transcript levels relative to those of medium-treated cells at 2 hours (HRS), the average value of which was taken as 1. The medium-treated groups in (b) and (c) are the same (SAA and Pg were tested together but were separated in the graphs for enhanced clarity). Data are means ± SD of duplicate determinations from one of three independent sets of experiments that yielded similar results.

    Journal: Clinical and Developmental Immunology

    Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue

    doi: 10.1155/2013/617809

    Figure Lengend Snippet: Regulation of Del-1 versus ICAM-1 and VCAM-1 by inflammatory stimuli. HUVEC were cultured for the indicated time intervals with 10 ng/mL TNF (a), 5 μ g/mL serum amyloid A (SAA; (b)), P. gingivalis (Pg; MOI = 10 : 1) (c), Pam 3 CSK 4 or LPS (both at 0.5 μ g/mL; (d)), 10 ng/mL IFN γ (e), or IL-17A or IL-17F (both at 10 ng/mL; (f)) and assayed for Del-1, ICAM-1, and VCAM-1 mRNA expression. Results were normalized to those of GAPDH mRNA and expressed as fold change in transcript levels relative to those of medium-treated cells at 2 hours (HRS), the average value of which was taken as 1. The medium-treated groups in (b) and (c) are the same (SAA and Pg were tested together but were separated in the graphs for enhanced clarity). Data are means ± SD of duplicate determinations from one of three independent sets of experiments that yielded similar results.

    Article Snippet: In new experiments in WT mice, we monitored the periodontal expression of Del-1 in parallel with ICAM-1, VCAM-1, and E-selectin from the age of 5 weeks to very old age (up to 24 months) ( ).

    Techniques: Cell Culture, Expressing

    Expression of endothelial adhesion molecules in Del-1 deficiency. (a) Gingiva dissected from 16-week-old C57BL/6 Edil 3 +/+ (WT) and Edil 3 −/− mice were processed for quantitative real-time PCR analysis of mRNA expression of the indicated genes; results were normalized to those of GAPDH mRNA and expressed as fold change in Edil 3 −/− transcript levels relative to WT, the average value of which was taken as 1. (b) Sagittal sections of interdental gingiva from 16-week-old C57BL/6 WT or Edil 3 −/− mice were stained for ICAM-1, VCAM-1, or E-selectin and CD31, as indicated. Shown are representative overlays of differential interference contrast and fluorescent confocal images, with colocalization demonstrated in merged images (scale bar, 50 μ m). (c) The fluorescence intensities of the images shown here and of additional representative images from independent mice (5 per group) were quantified using ImageJ analysis. In (a) and (c), data are means ± SD ( n = 5 mice per group). No statistically significant differences were detected between Edil 3 −/− and WT littermate controls.

    Journal: Clinical and Developmental Immunology

    Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue

    doi: 10.1155/2013/617809

    Figure Lengend Snippet: Expression of endothelial adhesion molecules in Del-1 deficiency. (a) Gingiva dissected from 16-week-old C57BL/6 Edil 3 +/+ (WT) and Edil 3 −/− mice were processed for quantitative real-time PCR analysis of mRNA expression of the indicated genes; results were normalized to those of GAPDH mRNA and expressed as fold change in Edil 3 −/− transcript levels relative to WT, the average value of which was taken as 1. (b) Sagittal sections of interdental gingiva from 16-week-old C57BL/6 WT or Edil 3 −/− mice were stained for ICAM-1, VCAM-1, or E-selectin and CD31, as indicated. Shown are representative overlays of differential interference contrast and fluorescent confocal images, with colocalization demonstrated in merged images (scale bar, 50 μ m). (c) The fluorescence intensities of the images shown here and of additional representative images from independent mice (5 per group) were quantified using ImageJ analysis. In (a) and (c), data are means ± SD ( n = 5 mice per group). No statistically significant differences were detected between Edil 3 −/− and WT littermate controls.

    Article Snippet: In new experiments in WT mice, we monitored the periodontal expression of Del-1 in parallel with ICAM-1, VCAM-1, and E-selectin from the age of 5 weeks to very old age (up to 24 months) ( ).

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