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    BioLegend cd31
    Cd31, supplied by BioLegend, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Biosynth Carbosynth antimicrobial substance 9 chloro 9 4 diethylaminophenyl 10phenylacridan
    Antimicrobial Substance 9 Chloro 9 4 Diethylaminophenyl 10phenylacridan, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Thermo Fisher anti pecam 1 mab
    MAC-1 interactions with ICAM-1 and ICAM-2 support luminal adhesion and crawling. The contribution of ICAM-1 and ICAM-2 ligation of leukocyte MAC-1 to IL-1β-stimulated adhesion, crawling and extravasation was investigated. WT or ICAM-2 −/− /LysM-EGFP +/− mice were pre-treated with anti-ICAM-1 or MAC-1 blocking mAb, or isotype control (3 mg per kg of body weight, i.v.). Tissues were labelled in vivo with an i.s. injection of fluorescent <t>anti-PECAM-1</t> mAb (4 µg i.s.), and co-injected with IL-1β (50 ng i.s.) 2 hours prior to exteriorisation. (A) The effect of genetic and pharmacological interventions was confirmed by capturing images at the end of the experiment (4 hours post stimulation) Scale bars: 10 µm. (B) The number of intravascular and extravasated neutrophils at this time point was quantified in each condition. Images and data are representative of three to five vessels per cremaster muscle ( n = 3–8 mice per group). (C) Sequential confocal images of selected venules were captured at 30-second intervals for ∼30 minutes per venule, from 2–4 hours post stimulation. Neutrophil crawling speed was quantified in IL-1β-stimulated animals pre-treated with blocking mAbs or isotype control. (D) The percentage of continuously or discontinuously crawling neutrophils per venule was determined in each group. Data were obtained from analysis of 66–113 crawling cells from four to nine vessels in four to eight mice. Results are mean ± s.e.m. for all events analysed. ** P
    Anti Pecam 1 Mab, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Thermo Fisher alexa fluor 555
    MAC-1 interactions with ICAM-1 and ICAM-2 support luminal adhesion and crawling. The contribution of ICAM-1 and ICAM-2 ligation of leukocyte MAC-1 to IL-1β-stimulated adhesion, crawling and extravasation was investigated. WT or ICAM-2 −/− /LysM-EGFP +/− mice were pre-treated with anti-ICAM-1 or MAC-1 blocking mAb, or isotype control (3 mg per kg of body weight, i.v.). Tissues were labelled in vivo with an i.s. injection of fluorescent <t>anti-PECAM-1</t> mAb (4 µg i.s.), and co-injected with IL-1β (50 ng i.s.) 2 hours prior to exteriorisation. (A) The effect of genetic and pharmacological interventions was confirmed by capturing images at the end of the experiment (4 hours post stimulation) Scale bars: 10 µm. (B) The number of intravascular and extravasated neutrophils at this time point was quantified in each condition. Images and data are representative of three to five vessels per cremaster muscle ( n = 3–8 mice per group). (C) Sequential confocal images of selected venules were captured at 30-second intervals for ∼30 minutes per venule, from 2–4 hours post stimulation. Neutrophil crawling speed was quantified in IL-1β-stimulated animals pre-treated with blocking mAbs or isotype control. (D) The percentage of continuously or discontinuously crawling neutrophils per venule was determined in each group. Data were obtained from analysis of 66–113 crawling cells from four to nine vessels in four to eight mice. Results are mean ± s.e.m. for all events analysed. ** P
    Alexa Fluor 555, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    MAC-1 interactions with ICAM-1 and ICAM-2 support luminal adhesion and crawling. The contribution of ICAM-1 and ICAM-2 ligation of leukocyte MAC-1 to IL-1β-stimulated adhesion, crawling and extravasation was investigated. WT or ICAM-2 −/− /LysM-EGFP +/− mice were pre-treated with anti-ICAM-1 or MAC-1 blocking mAb, or isotype control (3 mg per kg of body weight, i.v.). Tissues were labelled in vivo with an i.s. injection of fluorescent anti-PECAM-1 mAb (4 µg i.s.), and co-injected with IL-1β (50 ng i.s.) 2 hours prior to exteriorisation. (A) The effect of genetic and pharmacological interventions was confirmed by capturing images at the end of the experiment (4 hours post stimulation) Scale bars: 10 µm. (B) The number of intravascular and extravasated neutrophils at this time point was quantified in each condition. Images and data are representative of three to five vessels per cremaster muscle ( n = 3–8 mice per group). (C) Sequential confocal images of selected venules were captured at 30-second intervals for ∼30 minutes per venule, from 2–4 hours post stimulation. Neutrophil crawling speed was quantified in IL-1β-stimulated animals pre-treated with blocking mAbs or isotype control. (D) The percentage of continuously or discontinuously crawling neutrophils per venule was determined in each group. Data were obtained from analysis of 66–113 crawling cells from four to nine vessels in four to eight mice. Results are mean ± s.e.m. for all events analysed. ** P

    Journal: Journal of Cell Science

    Article Title: ICAM-2 facilitates luminal interactions between neutrophils and endothelial cells in vivo

    doi: 10.1242/jcs.137463

    Figure Lengend Snippet: MAC-1 interactions with ICAM-1 and ICAM-2 support luminal adhesion and crawling. The contribution of ICAM-1 and ICAM-2 ligation of leukocyte MAC-1 to IL-1β-stimulated adhesion, crawling and extravasation was investigated. WT or ICAM-2 −/− /LysM-EGFP +/− mice were pre-treated with anti-ICAM-1 or MAC-1 blocking mAb, or isotype control (3 mg per kg of body weight, i.v.). Tissues were labelled in vivo with an i.s. injection of fluorescent anti-PECAM-1 mAb (4 µg i.s.), and co-injected with IL-1β (50 ng i.s.) 2 hours prior to exteriorisation. (A) The effect of genetic and pharmacological interventions was confirmed by capturing images at the end of the experiment (4 hours post stimulation) Scale bars: 10 µm. (B) The number of intravascular and extravasated neutrophils at this time point was quantified in each condition. Images and data are representative of three to five vessels per cremaster muscle ( n = 3–8 mice per group). (C) Sequential confocal images of selected venules were captured at 30-second intervals for ∼30 minutes per venule, from 2–4 hours post stimulation. Neutrophil crawling speed was quantified in IL-1β-stimulated animals pre-treated with blocking mAbs or isotype control. (D) The percentage of continuously or discontinuously crawling neutrophils per venule was determined in each group. Data were obtained from analysis of 66–113 crawling cells from four to nine vessels in four to eight mice. Results are mean ± s.e.m. for all events analysed. ** P

    Article Snippet: Anti-ICAM-1 mAb (YN-1; rat IgG2b) and anti-PECAM-1 mAb (C390; rat IgG2a) were from eBiosciences (Hatfield, UK).

    Techniques: Ligation, Mouse Assay, Blocking Assay, In Vivo, Injection

    IL-1β-stimulated TEM dynamics in ICAM-2 KO and WT mice. The image sequences captured as described in Fig. 2 were also analysed for the occurrence of TEM. (A) The frequency at which TEM was observed following IL-1β stimulation was quantified in vessels from WT or ICAM-2 −/− /LysM-EGFP +/− mice over 30 minutes (the standard period of observation). (B) The route of TEM (paracellular or transcellular) was quantified as mean per venule. n = 60–196 cells from six to eight animals per group. (C) Crawling behaviour that preceded TEM (continuous or discontinuous) was quantified as mean per venule. n = 14–34 cells from six or seven animals per group. (D) The sequence of events from crawling through to completion of TEM was divided into three stages as illustrated. (i) Crawling: the period for which a neutrophil crawls within the lumen prior to reaching the site of TEM. (ii) Pre-TEM: the period for which a neutrophil interacts with the endothelial junction at the location of TEM prior to any visible disruption of the junctional integrity. (iii) TEM: the period from the first visible disruption of junctional PECAM-1 to the completion of migration to the sub-endothelial space. (E) The duration of stages i–iii as outlined in D was quantified. n = 14–34 cells (stage i), 23–76 cells (stage ii), or 20–99 cells (stage iii), from six or seven animals per group. (F) Periods of immobility were observed during luminal crawling ( Fig. 2E ), and the location of these events was analysed in relation to the location of EC junctions, and compared to the location of a random selection of normally crawling cells from the same vessels. n = 8 for WT and 77 for ICAM-2 KO immobile cells, and 250 randomly selected crawling cells from six or seven animals per group. (G) Examples of cells that were classified as being directly associated with EC junctions, and others that were only partially in contact with a junction, and not considered to be junction associated. Scale bars: 5 µm. Results are mean±s.e.m. ** P

    Journal: Journal of Cell Science

    Article Title: ICAM-2 facilitates luminal interactions between neutrophils and endothelial cells in vivo

    doi: 10.1242/jcs.137463

    Figure Lengend Snippet: IL-1β-stimulated TEM dynamics in ICAM-2 KO and WT mice. The image sequences captured as described in Fig. 2 were also analysed for the occurrence of TEM. (A) The frequency at which TEM was observed following IL-1β stimulation was quantified in vessels from WT or ICAM-2 −/− /LysM-EGFP +/− mice over 30 minutes (the standard period of observation). (B) The route of TEM (paracellular or transcellular) was quantified as mean per venule. n = 60–196 cells from six to eight animals per group. (C) Crawling behaviour that preceded TEM (continuous or discontinuous) was quantified as mean per venule. n = 14–34 cells from six or seven animals per group. (D) The sequence of events from crawling through to completion of TEM was divided into three stages as illustrated. (i) Crawling: the period for which a neutrophil crawls within the lumen prior to reaching the site of TEM. (ii) Pre-TEM: the period for which a neutrophil interacts with the endothelial junction at the location of TEM prior to any visible disruption of the junctional integrity. (iii) TEM: the period from the first visible disruption of junctional PECAM-1 to the completion of migration to the sub-endothelial space. (E) The duration of stages i–iii as outlined in D was quantified. n = 14–34 cells (stage i), 23–76 cells (stage ii), or 20–99 cells (stage iii), from six or seven animals per group. (F) Periods of immobility were observed during luminal crawling ( Fig. 2E ), and the location of these events was analysed in relation to the location of EC junctions, and compared to the location of a random selection of normally crawling cells from the same vessels. n = 8 for WT and 77 for ICAM-2 KO immobile cells, and 250 randomly selected crawling cells from six or seven animals per group. (G) Examples of cells that were classified as being directly associated with EC junctions, and others that were only partially in contact with a junction, and not considered to be junction associated. Scale bars: 5 µm. Results are mean±s.e.m. ** P

    Article Snippet: Anti-ICAM-1 mAb (YN-1; rat IgG2b) and anti-PECAM-1 mAb (C390; rat IgG2a) were from eBiosciences (Hatfield, UK).

    Techniques: Transmission Electron Microscopy, Mouse Assay, Sequencing, Migration, Selection

    PECAM-1 and ICAM-2 expression in cremasteric post-capillary venules. Venular expression and localisation of PECAM-1 and ICAM-2 was investigated in saline and IL-1β-stimulated WT or ICAM-2 KO tissues by immunofluorescence labelling and post-acquisition analysis of junctional and non-junctional regions of endothelial cells. (A) Representative images of venules from WT tissues which were labelled in vivo with an i.s. injection of fluorescent anti-PECAM-1 or anti-ICAM-2 mAb. Anti-ICAM-2 mAb specificity was confirmed by immunolabelling cremaster muscles from ICAM-2 KO mice. The brightly labelled perivascular structures are phagocytic cells, which non-specifically take up antibodies during the in vivo labelling protocol. Scale bars: 20 µm. (B) Linear transect intensity profile of a two-dimensional maximal intensity projection of a PECAM-1- and ICAM-2-labelled vessel, showing high intensity PECAM-1 peaks at the EC junctions. (C) Draq5 was used to label the nuclei of ICAM-2- and PECAM-1-labelled vessels, and high-magnification optical sections were examined to determine whether PECAM-1 and ICAM-2 were expressed on the luminal and/or abluminal side of the nucleus, indicating expression on the luminal or abluminal EC surface. (D) Junctional and non-junctional distribution of PECAM-1 and ICAM-2 was quantified from 3D models of IL-1β- or saline-stimulated vessels using Imaris software (see supplementary material Fig. S1B for the isosurface method). n = 3–5 vessels per mice, three mice per group, error bars show s.e.m. *** P

    Journal: Journal of Cell Science

    Article Title: ICAM-2 facilitates luminal interactions between neutrophils and endothelial cells in vivo

    doi: 10.1242/jcs.137463

    Figure Lengend Snippet: PECAM-1 and ICAM-2 expression in cremasteric post-capillary venules. Venular expression and localisation of PECAM-1 and ICAM-2 was investigated in saline and IL-1β-stimulated WT or ICAM-2 KO tissues by immunofluorescence labelling and post-acquisition analysis of junctional and non-junctional regions of endothelial cells. (A) Representative images of venules from WT tissues which were labelled in vivo with an i.s. injection of fluorescent anti-PECAM-1 or anti-ICAM-2 mAb. Anti-ICAM-2 mAb specificity was confirmed by immunolabelling cremaster muscles from ICAM-2 KO mice. The brightly labelled perivascular structures are phagocytic cells, which non-specifically take up antibodies during the in vivo labelling protocol. Scale bars: 20 µm. (B) Linear transect intensity profile of a two-dimensional maximal intensity projection of a PECAM-1- and ICAM-2-labelled vessel, showing high intensity PECAM-1 peaks at the EC junctions. (C) Draq5 was used to label the nuclei of ICAM-2- and PECAM-1-labelled vessels, and high-magnification optical sections were examined to determine whether PECAM-1 and ICAM-2 were expressed on the luminal and/or abluminal side of the nucleus, indicating expression on the luminal or abluminal EC surface. (D) Junctional and non-junctional distribution of PECAM-1 and ICAM-2 was quantified from 3D models of IL-1β- or saline-stimulated vessels using Imaris software (see supplementary material Fig. S1B for the isosurface method). n = 3–5 vessels per mice, three mice per group, error bars show s.e.m. *** P

    Article Snippet: Anti-ICAM-1 mAb (YN-1; rat IgG2b) and anti-PECAM-1 mAb (C390; rat IgG2a) were from eBiosciences (Hatfield, UK).

    Techniques: Expressing, Immunofluorescence, In Vivo, Injection, Mouse Assay, Software

    Role of ICAM-2 in IL-1β stimulated neutrophil luminal crawling dynamics. Cremasteric post-capillary venules of WT or ICAM-2 −/− /LysM-EGFP +/− mice, or WT LysM-EGFP +/− mice treated with anti-ICAM-2 blocking mAb (3 mg per kg of body weight, i.v.) were analysed. Tissues were labelled in vivo with an i.s. injection of fluorescent anti-PECAM-1 mAb (4 µg i.s.) and co-injected with IL-1β (50 ng i.s.) 2 hours prior to exteriorisation. Sequential confocal images of selected venules were captured at 30-second intervals, for ∼30 minutes per venule, for a further 2 hours. (A) The behaviour of luminal neutrophils was analysed, and the percentage of adherent neutrophils that exhibited crawling per venule was quantified. Crawling dynamics were also quantified from these sequences. Mean (B) duration, (C) speed, (D) speed on EC bodies (and supplementary material Fig. S3 ), and (E) speed variability (standard deviation of crawling speed per cell, divided by the mean crawling speed per cell) of crawling cells is shown. (F) The behaviour of crawling cells was identified as being either continuous or discontinuous, and the percentage of these behaviours among all crawling cells was quantified per vessel. Other crawling dynamics of continuously and discontinuously crawling cells was compared, and the mean (G) duration and (H) speed of continuously and discontinuously crawling cells in each mouse strain is shown. n = 76–81 cells (from 10 vessels) in six or seven mice per group, error bars show s.e.m. * P

    Journal: Journal of Cell Science

    Article Title: ICAM-2 facilitates luminal interactions between neutrophils and endothelial cells in vivo

    doi: 10.1242/jcs.137463

    Figure Lengend Snippet: Role of ICAM-2 in IL-1β stimulated neutrophil luminal crawling dynamics. Cremasteric post-capillary venules of WT or ICAM-2 −/− /LysM-EGFP +/− mice, or WT LysM-EGFP +/− mice treated with anti-ICAM-2 blocking mAb (3 mg per kg of body weight, i.v.) were analysed. Tissues were labelled in vivo with an i.s. injection of fluorescent anti-PECAM-1 mAb (4 µg i.s.) and co-injected with IL-1β (50 ng i.s.) 2 hours prior to exteriorisation. Sequential confocal images of selected venules were captured at 30-second intervals, for ∼30 minutes per venule, for a further 2 hours. (A) The behaviour of luminal neutrophils was analysed, and the percentage of adherent neutrophils that exhibited crawling per venule was quantified. Crawling dynamics were also quantified from these sequences. Mean (B) duration, (C) speed, (D) speed on EC bodies (and supplementary material Fig. S3 ), and (E) speed variability (standard deviation of crawling speed per cell, divided by the mean crawling speed per cell) of crawling cells is shown. (F) The behaviour of crawling cells was identified as being either continuous or discontinuous, and the percentage of these behaviours among all crawling cells was quantified per vessel. Other crawling dynamics of continuously and discontinuously crawling cells was compared, and the mean (G) duration and (H) speed of continuously and discontinuously crawling cells in each mouse strain is shown. n = 76–81 cells (from 10 vessels) in six or seven mice per group, error bars show s.e.m. * P

    Article Snippet: Anti-ICAM-1 mAb (YN-1; rat IgG2b) and anti-PECAM-1 mAb (C390; rat IgG2a) were from eBiosciences (Hatfield, UK).

    Techniques: Mouse Assay, Blocking Assay, In Vivo, Injection, Standard Deviation