Structured Review

Beckman Coulter icam 1
Effect of calcineurin inhibitors (CNIs) and FK565 on adhesion molecule expression on human coronary artery endothelial cells (HCAECs). (a) HCAECs were stimulated with cyclosporin A (CsA) or tacrolimus (Tac) and FK565. The frequencies of intercellular adhesion molecule‐1 <t>(ICAM‐1)‐</t> and vascular cell adhesion molecule‐1 (VCAM‐1)‐positive cells on HCAECs were measured by fluorescence activated cell sorter (FACS). The data are presented as the mean ± standard deviation (s.d.) ( n = 6). (b) HCAECs were stimulated with CsA or Tac and FK565. The mRNA expression of ICAM‐1, VCAM‐1 and E‐selectin in HCAECs was measured by a quantitative real‐time–polymerase chain reaction (PCR) analysis, and were normalized to those of β‐actin. The data are presented as the mean ± s.d. ( n = 3). * P
Icam 1, supplied by Beckman Coulter, used in various techniques. Bioz Stars score: 92/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "Calcineurin inhibitors exacerbate coronary arteritis via the MyD88 signalling pathway in a murine model of Kawasaki disease"

Article Title: Calcineurin inhibitors exacerbate coronary arteritis via the MyD88 signalling pathway in a murine model of Kawasaki disease

Journal: Clinical and Experimental Immunology

doi: 10.1111/cei.13002

Effect of calcineurin inhibitors (CNIs) and FK565 on adhesion molecule expression on human coronary artery endothelial cells (HCAECs). (a) HCAECs were stimulated with cyclosporin A (CsA) or tacrolimus (Tac) and FK565. The frequencies of intercellular adhesion molecule‐1 (ICAM‐1)‐ and vascular cell adhesion molecule‐1 (VCAM‐1)‐positive cells on HCAECs were measured by fluorescence activated cell sorter (FACS). The data are presented as the mean ± standard deviation (s.d.) ( n = 6). (b) HCAECs were stimulated with CsA or Tac and FK565. The mRNA expression of ICAM‐1, VCAM‐1 and E‐selectin in HCAECs was measured by a quantitative real‐time–polymerase chain reaction (PCR) analysis, and were normalized to those of β‐actin. The data are presented as the mean ± s.d. ( n = 3). * P
Figure Legend Snippet: Effect of calcineurin inhibitors (CNIs) and FK565 on adhesion molecule expression on human coronary artery endothelial cells (HCAECs). (a) HCAECs were stimulated with cyclosporin A (CsA) or tacrolimus (Tac) and FK565. The frequencies of intercellular adhesion molecule‐1 (ICAM‐1)‐ and vascular cell adhesion molecule‐1 (VCAM‐1)‐positive cells on HCAECs were measured by fluorescence activated cell sorter (FACS). The data are presented as the mean ± standard deviation (s.d.) ( n = 6). (b) HCAECs were stimulated with CsA or Tac and FK565. The mRNA expression of ICAM‐1, VCAM‐1 and E‐selectin in HCAECs was measured by a quantitative real‐time–polymerase chain reaction (PCR) analysis, and were normalized to those of β‐actin. The data are presented as the mean ± s.d. ( n = 3). * P

Techniques Used: Expressing, Fluorescence, FACS, Standard Deviation, Real-time Polymerase Chain Reaction, Polymerase Chain Reaction

2) Product Images from "JAK Inhibitors and Oxidative Stress Control"

Article Title: JAK Inhibitors and Oxidative Stress Control

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2019.02814

Effect of JAK inhibitors and NAC on ICAM-1 and PD-L1 induction mediated by IFNγ and H 2 O 2 . (A) Measurement of ROS in a time effect by flow cytometry after treatment with H 2 O 2 , IFNα, and IFNγ ( n = 3). (B) Dose effect of the JAK inhibitors AG490 and ruxotinib to reverse ICAM-1 induction mediated by IFNγ. (C) AG490, ruxolitinib, and NAC reverse H 2 O 2 -mediated induction of ICAM-1 ( n = 8). (D) AG490, ruxolitinib, and NAC reverse H 2 O 2 -mediated induction of PD-L1 ( n = 6). ICAM-1, intracellular adhesion molecule-1; NAC, N-acetylcysteine; PD-L1, programmed death ligand 1; ROS, reactive oxygen species; H 2 O 2 , hydrogen peroxide.
Figure Legend Snippet: Effect of JAK inhibitors and NAC on ICAM-1 and PD-L1 induction mediated by IFNγ and H 2 O 2 . (A) Measurement of ROS in a time effect by flow cytometry after treatment with H 2 O 2 , IFNα, and IFNγ ( n = 3). (B) Dose effect of the JAK inhibitors AG490 and ruxotinib to reverse ICAM-1 induction mediated by IFNγ. (C) AG490, ruxolitinib, and NAC reverse H 2 O 2 -mediated induction of ICAM-1 ( n = 8). (D) AG490, ruxolitinib, and NAC reverse H 2 O 2 -mediated induction of PD-L1 ( n = 6). ICAM-1, intracellular adhesion molecule-1; NAC, N-acetylcysteine; PD-L1, programmed death ligand 1; ROS, reactive oxygen species; H 2 O 2 , hydrogen peroxide.

Techniques Used: Flow Cytometry, Cytometry

Expression of ICAM-1 and PD-L1 measured by real-time PCR and flow cytometry in the human salivary gland (HSG) cell line after 48 h of treatment with H 2 O 2 , IFNα, and IFNγ, respectively. (A,B) H 2 O 2 dose effect on ICAM-1 and PD-L1 mRA expression ( n = 3). (C,D) HSG (no treatment), H 2 O 2 (150 μM), IFNα, and IFNγ effect on ICAM-1 and PD-L1 mRA expression ( n = 3). (E,F) No treatment ( n = 17 and 10, respectively), H 2 O 2 ( n = 20 and 11), IFNα ( n = 14 and 9), and IFNγ ( n = 9 both) effect on cell surface ICAM-1 and PD-L1 expression as evaluated by flow cytometry. MFI, mean fluorescence intensity; ICAM-1, intracellular adhesion molecule-1; PD-L1, programmed death ligand 1.
Figure Legend Snippet: Expression of ICAM-1 and PD-L1 measured by real-time PCR and flow cytometry in the human salivary gland (HSG) cell line after 48 h of treatment with H 2 O 2 , IFNα, and IFNγ, respectively. (A,B) H 2 O 2 dose effect on ICAM-1 and PD-L1 mRA expression ( n = 3). (C,D) HSG (no treatment), H 2 O 2 (150 μM), IFNα, and IFNγ effect on ICAM-1 and PD-L1 mRA expression ( n = 3). (E,F) No treatment ( n = 17 and 10, respectively), H 2 O 2 ( n = 20 and 11), IFNα ( n = 14 and 9), and IFNγ ( n = 9 both) effect on cell surface ICAM-1 and PD-L1 expression as evaluated by flow cytometry. MFI, mean fluorescence intensity; ICAM-1, intracellular adhesion molecule-1; PD-L1, programmed death ligand 1.

Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Flow Cytometry, Cytometry, Fluorescence

Phosphorylation status of pSTAT1 Y701 and pSTAT3 Y705 measured by WB ( n = 3 each). (A) WB showing the expression of pSTAT1, pSTAT3, and total STAT1 after 48 h of treatment with increasing concentrations of H 2 O 2 . H 2 O 2 increases pSTAT3 with the optimal effect observed at 150 μM, whereas no effect is observed on the expression of pSTAT1. (B) WB showing expression of pSTAT3 after 48 h of treatment with 150 μM of H 2 O 2 with and without two JAK(1)/2 inhibitors, AG490 40 μM, a JAK2 inhibitor, ruxolitinib 100 nM a JAK1/2 inhibitor and NAC 50 mM. Both JAK1/2 inhibitors and NAC reverse H 2 O 2 -mediated induction of pSTAT3. (C) ROS induction mediated by H 2 O 2 phosphorylates STAT3, a process that is reversed by NAC and JAK(1)/2 inhibitors. ROS, reactive oxygen species; H 2 O 2 , hydrogen peroxide; JAK, Janus kinase; STAT, signal transducer and activator of transcription; ICAM-1, intracellular adhesion molecule-1; PD-L1, programmed death ligand 1; WB, Western blot.
Figure Legend Snippet: Phosphorylation status of pSTAT1 Y701 and pSTAT3 Y705 measured by WB ( n = 3 each). (A) WB showing the expression of pSTAT1, pSTAT3, and total STAT1 after 48 h of treatment with increasing concentrations of H 2 O 2 . H 2 O 2 increases pSTAT3 with the optimal effect observed at 150 μM, whereas no effect is observed on the expression of pSTAT1. (B) WB showing expression of pSTAT3 after 48 h of treatment with 150 μM of H 2 O 2 with and without two JAK(1)/2 inhibitors, AG490 40 μM, a JAK2 inhibitor, ruxolitinib 100 nM a JAK1/2 inhibitor and NAC 50 mM. Both JAK1/2 inhibitors and NAC reverse H 2 O 2 -mediated induction of pSTAT3. (C) ROS induction mediated by H 2 O 2 phosphorylates STAT3, a process that is reversed by NAC and JAK(1)/2 inhibitors. ROS, reactive oxygen species; H 2 O 2 , hydrogen peroxide; JAK, Janus kinase; STAT, signal transducer and activator of transcription; ICAM-1, intracellular adhesion molecule-1; PD-L1, programmed death ligand 1; WB, Western blot.

Techniques Used: Western Blot, Expressing

ROS contribute to ICAM-1 and PD-L1 induction in salivary gland epithelial cells through a JAK(1/)2/STAT3 pathway. ICAM-1 upregulation leads to SGEC activation and induces lymphocytic infiltration. PD-L1 reduces T-cell activation and IFNγ production on one hand but, on the other hand, contributes to SGECs activation and disease perpetuation as it increases salivary gland epithelial cell survival and reduces pro-inflammatory TH1 cell-mediated activation and toxicity. JAK(1/)2 inhibitors, AG490 and ruxolitinib, as well as NAC reverse this process as described in Figure 3 . IFN(α/γ), interferon α/γ, ICAM-1, intracellular adhesion molecule-1; PD-L1, programmed death ligand 1; TH1, T helper 1 lymphocyte; ROS, reactive oxygen species; H 2 O 2 , hydrogen peroxide; TYK, tyrosine kinase; JAK, janus kinase; STAT, signal transducer and activator of transcription.
Figure Legend Snippet: ROS contribute to ICAM-1 and PD-L1 induction in salivary gland epithelial cells through a JAK(1/)2/STAT3 pathway. ICAM-1 upregulation leads to SGEC activation and induces lymphocytic infiltration. PD-L1 reduces T-cell activation and IFNγ production on one hand but, on the other hand, contributes to SGECs activation and disease perpetuation as it increases salivary gland epithelial cell survival and reduces pro-inflammatory TH1 cell-mediated activation and toxicity. JAK(1/)2 inhibitors, AG490 and ruxolitinib, as well as NAC reverse this process as described in Figure 3 . IFN(α/γ), interferon α/γ, ICAM-1, intracellular adhesion molecule-1; PD-L1, programmed death ligand 1; TH1, T helper 1 lymphocyte; ROS, reactive oxygen species; H 2 O 2 , hydrogen peroxide; TYK, tyrosine kinase; JAK, janus kinase; STAT, signal transducer and activator of transcription.

Techniques Used: Activation Assay

Related Articles

Enzyme-linked Immunosorbent Assay:

Article Title: Down-regulation of lncRNA MALAT1 alleviates vascular lesion and vascular remodeling of rats with hypertension
Article Snippet: .. Measurement of serum factors After three-week intervention treatment, 5 mL blood of abdominal aorta collected from the rats was placed for 30 min, centrifuged for 10 min at 3000 r/min and the supernatant was adopted, enzyme-linked immunosorbent assay (ELISA) was used to evaluate the content of tumor necrosis factor-α(TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), monocyte chemotactic protein-1 (MCP-1), Ang II, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and endothelin-1 (ET-1) according to the instruction of the kits purchased from Beckman Coulter, Inc. (CA, USA). .. The content of nitric oxide (NO) was detected by nitric reductase method, the content of reactive oxygen species (ROS) was measured by colorimetry, the content of malondialdehyde (MDA) was evaluated by thiobarbituric acid and the content of superoxide dismutase (SOD) was detected by xanthine oxidase method, the reagent used for testing NO, ROS, MDA and SOD were all purchased from Jingmei Bioengineering Co., Ltd., (Shenzhen, China).

Flow Cytometry:

Article Title: Calcineurin inhibitors exacerbate coronary arteritis via the MyD88 signalling pathway in a murine model of Kawasaki disease
Article Snippet: .. The expression of ICAM‐1 and VCAM‐1 was analysed using an EPICS XL flow cytometer (Beckman Coulter). .. The data were analysed with the Kaluza software program, version 1.5 (Beckman Coulter).

Cytometry:

Article Title: Calcineurin inhibitors exacerbate coronary arteritis via the MyD88 signalling pathway in a murine model of Kawasaki disease
Article Snippet: .. The expression of ICAM‐1 and VCAM‐1 was analysed using an EPICS XL flow cytometer (Beckman Coulter). .. The data were analysed with the Kaluza software program, version 1.5 (Beckman Coulter).

Expressing:

Article Title: Calcineurin inhibitors exacerbate coronary arteritis via the MyD88 signalling pathway in a murine model of Kawasaki disease
Article Snippet: .. The expression of ICAM‐1 and VCAM‐1 was analysed using an EPICS XL flow cytometer (Beckman Coulter). .. The data were analysed with the Kaluza software program, version 1.5 (Beckman Coulter).

Article Title: JAK Inhibitors and Oxidative Stress Control
Article Snippet: .. Afterward, the effect on ICAM-1 and PD-L1 plasma membrane expression was evaluated using ICAM-1 (CD54)-FITC (Beckman Coulter, Brea, CA) and PD-L1 (CD274)-PE (Thermo Fisher Scientific, Waltham, US) anti-mouse antibodies. ..

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    Beckman Coulter icam 1
    Hemolysis inducing renal injury. Kinetics of mRNA levels in renal tissue of (A) NGAL, (B) Kim-1, (C) Ki-67, (D) IL-6, (E) E-selectin, (F) P-selectin and (G) <t>ICAM-1</t> at 1, 2, and 4 days after PBS or phenylhydrazine (PHZ) injection. (H) Human umbilical vein endothelial cells (HUVECs) were incubated for 24 h with increased concentration of PHZ in M199 medium, containing 20% fetal calf serum, and cell death was measured by double staining with annexin-V and DAPI by flow cytometry. (I–K) HUVECs were incubated for 24 h with increased concentration of PHZ or TNF-α as a positive control, in M199 medium, containing 20% fetal calf serum. E-selectin (I) , VCAM-1 (J) , and ICAM-1 (K) were measured by flow cytometry. Data are presented for 0.312-mg/mL PHZ, gating on live (annexin-V − , DAPI − cells, about 80% of the total cell population). Mean ± SEM, * p
    Icam 1, supplied by Beckman Coulter, used in various techniques. Bioz Stars score: 92/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 92 stars, based on 13 article reviews
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    92/100 stars
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    Beckman Coulter human icam 1
    Immunofluorescence analysis of endothelial markers on subcutaneous fat and brain-derived EC CM monolayers. The figure shows evidence for the expression of several typical endothelial markers on submembrane or cell type surface, including vWF, CD31, ZO-1, <t>ICAM-1,</t> CD36 and CD62-E. Micrographs presented here are from patient PM91-derived cells in passage 3 and are representative of the results obtained with all the other CM patients. Magnification: × 100 for general morphology micrographs, × 400 for immunofluorescence micrographs.
    Human Icam 1, supplied by Beckman Coulter, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human icam 1/product/Beckman Coulter
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    human icam 1 - by Bioz Stars, 2020-09
    90/100 stars
      Buy from Supplier

    Image Search Results


    Hemolysis inducing renal injury. Kinetics of mRNA levels in renal tissue of (A) NGAL, (B) Kim-1, (C) Ki-67, (D) IL-6, (E) E-selectin, (F) P-selectin and (G) ICAM-1 at 1, 2, and 4 days after PBS or phenylhydrazine (PHZ) injection. (H) Human umbilical vein endothelial cells (HUVECs) were incubated for 24 h with increased concentration of PHZ in M199 medium, containing 20% fetal calf serum, and cell death was measured by double staining with annexin-V and DAPI by flow cytometry. (I–K) HUVECs were incubated for 24 h with increased concentration of PHZ or TNF-α as a positive control, in M199 medium, containing 20% fetal calf serum. E-selectin (I) , VCAM-1 (J) , and ICAM-1 (K) were measured by flow cytometry. Data are presented for 0.312-mg/mL PHZ, gating on live (annexin-V − , DAPI − cells, about 80% of the total cell population). Mean ± SEM, * p

    Journal: Frontiers in Immunology

    Article Title: Characterization of Renal Injury and Inflammation in an Experimental Model of Intravascular Hemolysis

    doi: 10.3389/fimmu.2018.00179

    Figure Lengend Snippet: Hemolysis inducing renal injury. Kinetics of mRNA levels in renal tissue of (A) NGAL, (B) Kim-1, (C) Ki-67, (D) IL-6, (E) E-selectin, (F) P-selectin and (G) ICAM-1 at 1, 2, and 4 days after PBS or phenylhydrazine (PHZ) injection. (H) Human umbilical vein endothelial cells (HUVECs) were incubated for 24 h with increased concentration of PHZ in M199 medium, containing 20% fetal calf serum, and cell death was measured by double staining with annexin-V and DAPI by flow cytometry. (I–K) HUVECs were incubated for 24 h with increased concentration of PHZ or TNF-α as a positive control, in M199 medium, containing 20% fetal calf serum. E-selectin (I) , VCAM-1 (J) , and ICAM-1 (K) were measured by flow cytometry. Data are presented for 0.312-mg/mL PHZ, gating on live (annexin-V − , DAPI − cells, about 80% of the total cell population). Mean ± SEM, * p

    Article Snippet: For the ICAM-1 and P-selectin staining, a goat anti-mouse PE antibody 1:100 (Beckman, IM0855)was used for 30 min at 4°C.

    Techniques: Injection, Incubation, Concentration Assay, Double Staining, Flow Cytometry, Cytometry, Positive Control

    The renal injury which is largely heme-independent. mRNA levels of NGAL (A) , Kim-1 (B) , and IL-6 (C) in renal tissue after injection of heme at day 2. Influence of hemopexin (Hx) on mRNA level in the phenylhydrazine (PHZ) model, (D) NGAL, (E) Kim-1, (F) IL-6, (G) E-selectin, (H) P-selectin, and (I) ICAM-1 at day 1 or day 4, as mentioned under the panels. * p

    Journal: Frontiers in Immunology

    Article Title: Characterization of Renal Injury and Inflammation in an Experimental Model of Intravascular Hemolysis

    doi: 10.3389/fimmu.2018.00179

    Figure Lengend Snippet: The renal injury which is largely heme-independent. mRNA levels of NGAL (A) , Kim-1 (B) , and IL-6 (C) in renal tissue after injection of heme at day 2. Influence of hemopexin (Hx) on mRNA level in the phenylhydrazine (PHZ) model, (D) NGAL, (E) Kim-1, (F) IL-6, (G) E-selectin, (H) P-selectin, and (I) ICAM-1 at day 1 or day 4, as mentioned under the panels. * p

    Article Snippet: For the ICAM-1 and P-selectin staining, a goat anti-mouse PE antibody 1:100 (Beckman, IM0855)was used for 30 min at 4°C.

    Techniques: Injection

    Consequences of interactions of neutrophils with platelets for the extravasation of neutrophils. Binding of ICAM-1/CD54 or VCAM-1/CD106 to neutrophils isolated from the peripheral blood of WT mice was assessed upon exposure to recombinant murine CD40L/CD154, P-selectin/CD62P, L-selectin/CD62L, or PSGL-1/CD162 by flow cytometry. P-selectin-elicited binding of ICAM-1/CD54 to murine neutrophils was quantified upon blockade of PSGL-1/CD162 or inhibition of MAPK ( A , upper panels; mean ± SEM; n = 4–6 per group; # p

    Journal: PLoS Biology

    Article Title: Platelets Guide Leukocytes to Their Sites of Extravasation

    doi: 10.1371/journal.pbio.1002459

    Figure Lengend Snippet: Consequences of interactions of neutrophils with platelets for the extravasation of neutrophils. Binding of ICAM-1/CD54 or VCAM-1/CD106 to neutrophils isolated from the peripheral blood of WT mice was assessed upon exposure to recombinant murine CD40L/CD154, P-selectin/CD62P, L-selectin/CD62L, or PSGL-1/CD162 by flow cytometry. P-selectin-elicited binding of ICAM-1/CD54 to murine neutrophils was quantified upon blockade of PSGL-1/CD162 or inhibition of MAPK ( A , upper panels; mean ± SEM; n = 4–6 per group; # p

    Article Snippet: Binding of ICAM-1 or VCAM-1 was measured by a flow cytometer (Gallios, Beckmann Coulter).

    Techniques: Binding Assay, Isolation, Mouse Assay, Recombinant, Flow Cytometry, Cytometry, Inhibition

    Endothelial expression of adhesion and signaling molecules, composition of the vascular wall, and shear rates in the venular microvasculature. Representative confocal microscopy images of ICAM-1/CD54, VCAM-1/CD106, ICAM-2/CD102, PECAM-1/CD31, JAM-A, and CCL2 expression in venular endothelial cells of the cremaster muscle of WT mice before (open dots) and after (filled dots) stimulation with CCL2 ( A ; scale bar 50 μm). Panels show quantitative expression levels of these proteins in dependency of the venular diameter as well as the corresponding venular shear rates (mean ± SEM; n = 3–4 per group; # p

    Journal: PLoS Biology

    Article Title: Platelets Guide Leukocytes to Their Sites of Extravasation

    doi: 10.1371/journal.pbio.1002459

    Figure Lengend Snippet: Endothelial expression of adhesion and signaling molecules, composition of the vascular wall, and shear rates in the venular microvasculature. Representative confocal microscopy images of ICAM-1/CD54, VCAM-1/CD106, ICAM-2/CD102, PECAM-1/CD31, JAM-A, and CCL2 expression in venular endothelial cells of the cremaster muscle of WT mice before (open dots) and after (filled dots) stimulation with CCL2 ( A ; scale bar 50 μm). Panels show quantitative expression levels of these proteins in dependency of the venular diameter as well as the corresponding venular shear rates (mean ± SEM; n = 3–4 per group; # p

    Article Snippet: Binding of ICAM-1 or VCAM-1 was measured by a flow cytometer (Gallios, Beckmann Coulter).

    Techniques: Expressing, Confocal Microscopy, Mouse Assay

    LTB 4 induces increased surface expression of ICAM-1 on HMVECs

    Journal: Shock (Augusta, Ga.)

    Article Title: Leukotriene B4 and its Metabolites Prime the Neutrophil Oxidase and Induce Pro-Inflammatory Activation of Human Pulmonary Microvascular Endothelial Cells

    doi: 10.1097/SHK.0b013e3181faceb3

    Figure Lengend Snippet: LTB 4 induces increased surface expression of ICAM-1 on HMVECs

    Article Snippet: At 10 μM LTB4 and its metabolites: 6-trans-LTB4 , 20-OH-LTB4 and 20-COOH-LTB4 all elicited increased surface expression of ICAM-1 as compared to albumin-treated controls ( ).

    Techniques: Expressing

    Immunofluorescence analysis of endothelial markers on subcutaneous fat and brain-derived EC CM monolayers. The figure shows evidence for the expression of several typical endothelial markers on submembrane or cell type surface, including vWF, CD31, ZO-1, ICAM-1, CD36 and CD62-E. Micrographs presented here are from patient PM91-derived cells in passage 3 and are representative of the results obtained with all the other CM patients. Magnification: × 100 for general morphology micrographs, × 400 for immunofluorescence micrographs.

    Journal: Cellular Microbiology

    Article Title: Vascular endothelial cells cultured from patients with cerebral or uncomplicated malaria exhibit differential reactivity to TNF

    doi: 10.1111/j.1462-5822.2010.01528.x

    Figure Lengend Snippet: Immunofluorescence analysis of endothelial markers on subcutaneous fat and brain-derived EC CM monolayers. The figure shows evidence for the expression of several typical endothelial markers on submembrane or cell type surface, including vWF, CD31, ZO-1, ICAM-1, CD36 and CD62-E. Micrographs presented here are from patient PM91-derived cells in passage 3 and are representative of the results obtained with all the other CM patients. Magnification: × 100 for general morphology micrographs, × 400 for immunofluorescence micrographs.

    Article Snippet: Cells were then incubated, respectively, with monoclonal antibodies to human ICAM-1, VCAM-1, CD61 (Beckman-Coulter Immunotech) and CD62-E (Serotec), all at 10 µg ml−1 for 40 min at room temperature.

    Techniques: Immunofluorescence, Derivative Assay, Expressing

    Comparison of TNF-induced adhesion molecule upregulation between EC UM and EC CM of subcutaneous fat origin. Cells were seeded in a 96-well plate and stimulated by increasing concentrations of TNF. EC UM and EC CM were then fixed and the expression of ICAM-1, VCAM-1 and CD61 was measured by cell-based ELISA (A, B and C respectively). Results are expressed as mean ± SD of two experiments (Dunn's test, * P

    Journal: Cellular Microbiology

    Article Title: Vascular endothelial cells cultured from patients with cerebral or uncomplicated malaria exhibit differential reactivity to TNF

    doi: 10.1111/j.1462-5822.2010.01528.x

    Figure Lengend Snippet: Comparison of TNF-induced adhesion molecule upregulation between EC UM and EC CM of subcutaneous fat origin. Cells were seeded in a 96-well plate and stimulated by increasing concentrations of TNF. EC UM and EC CM were then fixed and the expression of ICAM-1, VCAM-1 and CD61 was measured by cell-based ELISA (A, B and C respectively). Results are expressed as mean ± SD of two experiments (Dunn's test, * P

    Article Snippet: Cells were then incubated, respectively, with monoclonal antibodies to human ICAM-1, VCAM-1, CD61 (Beckman-Coulter Immunotech) and CD62-E (Serotec), all at 10 µg ml−1 for 40 min at room temperature.

    Techniques: Expressing, In-Cell ELISA