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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
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Images

1) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

2) Product Images from "Circulating Extracellular Vesicles with Specific Proteome and Liver MicroRNAs Are Potential Biomarkers for Liver Injury in Experimental Fatty Liver Disease"

Article Title: Circulating Extracellular Vesicles with Specific Proteome and Liver MicroRNAs Are Potential Biomarkers for Liver Injury in Experimental Fatty Liver Disease

Journal: PLoS ONE

doi: 10.1371/journal.pone.0113651

Characterization of circulating extracellular vesicles (EV) in a diet-induced NASH model. ( A ) Dynamic light scattering analysis was performed to determine the size of EVs isolated from the platelet-free plasma of CDAA-fed mice for 20 weeks. The graph shows a predominant peak of big vesicles (mean 630 nm) corresponding to microparticles and a peak of smaller vesicles (mean 100 nm), corresponding to exosomes. ( B ) Exosomes (EXO) and microparticles (MP) were separated from the whole EV population and markers of EXO (Cd63, Cd81, ICAM-1), MP (Vanin-1 and Annexin V) and the hepatocyte-specific asialoglycoprotein-receptor (ASGPR1) were identified by western blot analysis. ( C ) Representative TEM macro photograph of circulating EVs isolated from platelet-free plasma of CDAA-fed mice for 20 weeks. ( D ) Flow cytometry analysis of circulating AnnexinV+ microparticles per µL of platelet-free plasma isolated from CDAA (CD), CSAA (CS) or chow diet fed mice for 20 weeks. *P
Figure Legend Snippet: Characterization of circulating extracellular vesicles (EV) in a diet-induced NASH model. ( A ) Dynamic light scattering analysis was performed to determine the size of EVs isolated from the platelet-free plasma of CDAA-fed mice for 20 weeks. The graph shows a predominant peak of big vesicles (mean 630 nm) corresponding to microparticles and a peak of smaller vesicles (mean 100 nm), corresponding to exosomes. ( B ) Exosomes (EXO) and microparticles (MP) were separated from the whole EV population and markers of EXO (Cd63, Cd81, ICAM-1), MP (Vanin-1 and Annexin V) and the hepatocyte-specific asialoglycoprotein-receptor (ASGPR1) were identified by western blot analysis. ( C ) Representative TEM macro photograph of circulating EVs isolated from platelet-free plasma of CDAA-fed mice for 20 weeks. ( D ) Flow cytometry analysis of circulating AnnexinV+ microparticles per µL of platelet-free plasma isolated from CDAA (CD), CSAA (CS) or chow diet fed mice for 20 weeks. *P

Techniques Used: Isolation, Mouse Assay, Western Blot, Transmission Electron Microscopy, Flow Cytometry, Cytometry

3) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

4) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

5) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

6) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

7) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

8) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

9) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

10) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

11) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

12) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

13) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

14) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

15) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

16) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

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

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

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
Figure Legend 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

Techniques Used: 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.
Figure Legend 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.

Techniques Used: 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.
Figure Legend 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.

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

Related Articles

Blocking Assay:

Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue
Article Snippet: .. Using a similar system, we determined whether immobilized ICAM-1 could induce chemokine production in ATRA-differentiated HL-60 neutrophils, and, if so, whether soluble Del-1 could block ICAM-1–dependent chemokine production. .. In our experiments, ICAM-1 was used as a fusion protein with IgG Fc (ICAM-1-Fc) and was coated on plates treated with anti-Fc antibodies.

Mouse Assay:

Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue
Article Snippet: .. The observation that the periodontal bone loss in aging WT mice correlates with significant changes in the expression of Del-1, but not of ICAM-1, VCAM1, or E-selectin, further supports the notion that the age-associated Del-1 deficiency is an important determinant of age-associated periodontitis. .. Del-1 Inhibits ICAM-1-Dependent Chemokine Production by Neutrophils The interaction of endothelial ICAM-1 with β 2 integrins in monocytes was shown to induce the release of chemokine C-C ligand 3 (CCL3; also known as macrophage inflammatory protein-1α ) [ ].

Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue
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) ( ). .. As expected, the expression of Del-1 significantly declined as a function of age; however, the expression of the three adhesion molecules was not significantly altered ( ).

Incubation:

Article Title: Circulating Extracellular Vesicles with Specific Proteome and Liver MicroRNAs Are Potential Biomarkers for Liver Injury in Experimental Fatty Liver Disease
Article Snippet: .. Primary rabbit polyclonal antibody anti-mouse Vanin-1 (1∶500; Proteintech, Chicago, IL, USA), Cd63, Cd81, ASGPR1 (1∶1000; Genetex, Irvine, CA, USA) and Icam-1 (1∶1000; Abnova, Taipei city, Taiwan) were incubated overnight at 4°C. .. Proteins were visualized by Supersignal West Pico chemiluminescence substrate (Pierce biotechnology, Rockford, IL, USA) and quantified by ImageJ software.

other:

Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue
Article Snippet: Del-1 Inhibits ICAM-1-Dependent Chemokine Production by Neutrophils The interaction of endothelial ICAM-1 with β 2 integrins in monocytes was shown to induce the release of chemokine C-C ligand 3 (CCL3; also known as macrophage inflammatory protein-1α ) [ ].

Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue
Article Snippet: TNF inhibited Del-1 and strongly upregulated ICAM-1 and VCAM-1 at all three time intervals examined (2, 4, and 16 hours) ( ).

Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue
Article Snippet: Firm adhesion and crawling are primarily mediated by leukocyte integrins that interact with endothelial counterreceptors such as VCAM-1 and ICAM-1 [ , , ].

Expressing:

Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue
Article Snippet: .. The observation that the periodontal bone loss in aging WT mice correlates with significant changes in the expression of Del-1, but not of ICAM-1, VCAM1, or E-selectin, further supports the notion that the age-associated Del-1 deficiency is an important determinant of age-associated periodontitis. .. Del-1 Inhibits ICAM-1-Dependent Chemokine Production by Neutrophils The interaction of endothelial ICAM-1 with β 2 integrins in monocytes was shown to induce the release of chemokine C-C ligand 3 (CCL3; also known as macrophage inflammatory protein-1α ) [ ].

Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue
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) ( ). .. As expected, the expression of Del-1 significantly declined as a function of age; however, the expression of the three adhesion molecules was not significantly altered ( ).

Staining:

Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue
Article Snippet: .. Serial mesiodistal sections parallel to the long axis of the teeth (sagittal) were stained using monoclonal antibodies to ICAM-1 (YN1/1.7.4; Abnova), VCAM-1 (MVCAM. .. A [429]; BioLegend), or with polyclonal antibodies to CD31 or E-selectin (both from LSBio), followed by secondary reagents (AlexaFluor488- or AlexaFluor594-conjugated goat anti-rabbit IgG; Molecular Probes).

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    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
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    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: Firm adhesion and crawling are primarily mediated by leukocyte integrins that interact with endothelial counterreceptors such as VCAM-1 and ICAM-1 [ , , ].

    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: Firm adhesion and crawling are primarily mediated by leukocyte integrins that interact with endothelial counterreceptors such as VCAM-1 and ICAM-1 [ , , ].

    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: Firm adhesion and crawling are primarily mediated by leukocyte integrins that interact with endothelial counterreceptors such as VCAM-1 and ICAM-1 [ , , ].

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

    Characterization of circulating extracellular vesicles (EV) in a diet-induced NASH model. ( A ) Dynamic light scattering analysis was performed to determine the size of EVs isolated from the platelet-free plasma of CDAA-fed mice for 20 weeks. The graph shows a predominant peak of big vesicles (mean 630 nm) corresponding to microparticles and a peak of smaller vesicles (mean 100 nm), corresponding to exosomes. ( B ) Exosomes (EXO) and microparticles (MP) were separated from the whole EV population and markers of EXO (Cd63, Cd81, ICAM-1), MP (Vanin-1 and Annexin V) and the hepatocyte-specific asialoglycoprotein-receptor (ASGPR1) were identified by western blot analysis. ( C ) Representative TEM macro photograph of circulating EVs isolated from platelet-free plasma of CDAA-fed mice for 20 weeks. ( D ) Flow cytometry analysis of circulating AnnexinV+ microparticles per µL of platelet-free plasma isolated from CDAA (CD), CSAA (CS) or chow diet fed mice for 20 weeks. *P

    Journal: PLoS ONE

    Article Title: Circulating Extracellular Vesicles with Specific Proteome and Liver MicroRNAs Are Potential Biomarkers for Liver Injury in Experimental Fatty Liver Disease

    doi: 10.1371/journal.pone.0113651

    Figure Lengend Snippet: Characterization of circulating extracellular vesicles (EV) in a diet-induced NASH model. ( A ) Dynamic light scattering analysis was performed to determine the size of EVs isolated from the platelet-free plasma of CDAA-fed mice for 20 weeks. The graph shows a predominant peak of big vesicles (mean 630 nm) corresponding to microparticles and a peak of smaller vesicles (mean 100 nm), corresponding to exosomes. ( B ) Exosomes (EXO) and microparticles (MP) were separated from the whole EV population and markers of EXO (Cd63, Cd81, ICAM-1), MP (Vanin-1 and Annexin V) and the hepatocyte-specific asialoglycoprotein-receptor (ASGPR1) were identified by western blot analysis. ( C ) Representative TEM macro photograph of circulating EVs isolated from platelet-free plasma of CDAA-fed mice for 20 weeks. ( D ) Flow cytometry analysis of circulating AnnexinV+ microparticles per µL of platelet-free plasma isolated from CDAA (CD), CSAA (CS) or chow diet fed mice for 20 weeks. *P

    Article Snippet: Primary rabbit polyclonal antibody anti-mouse Vanin-1 (1∶500; Proteintech, Chicago, IL, USA), Cd63, Cd81, ASGPR1 (1∶1000; Genetex, Irvine, CA, USA) and Icam-1 (1∶1000; Abnova, Taipei city, Taiwan) were incubated overnight at 4°C.

    Techniques: Isolation, Mouse Assay, Western Blot, Transmission Electron Microscopy, Flow Cytometry, Cytometry