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Description (A) and characterization of endothelial cell ( ec PD-L1 −/− ) (B, D) or neutrophil ( pmn PD-L1 −/− ) (C, E) restricted constitutive PD-L1 gene-deficient mice. Taconic Knockout Repository [mouse TF0103 (MGI:1926446); Taconic Biosciences Inc., Germantown, NY], CD274/PD-L1 conditional knockout mouse. PD-L1 gene exons 1 to 4 are shown as green boxes and loxP sites flanking exon 2 are depicted as red triangles (A) . Homozygous PD-L1 flox/flox were subsequently crossed <t>to</t> <t>either</t> <t>VE-Cadherin‐Cre</t> (B6.FVB-Tg[Cdh5-cre]7Mlia/J; Strain #:006137; RRID: IMSR_JAX:006137) or the S100a8-Cre (B6.Cg-Tg[S100a8-cre,-EGFP]1IIw/J; Strain #:021614; RRID: IMSR_JAX:021614) mice, obtained from Jackson Labs, to produce either mice homozygous for both the flox PD-L1 and specific cell-lineage Cre promoter genes or mice that were heterozygous for one or both genes that served as “Controls”. Gating strategy and typical flow cytogram/dot plot of select cell-lineage restricted PD-L1 expression [either CD31 and PD-L1 (B) or Ly6G and PD-L1 (C) ] for various breeding outcomes from respective Cre-Lox matings for PD-L1 flox/flox animals with VE-Cadherin‐Cre (B) or PD-L1 flox/flox animals with S100a8-Cre (C) . Summary data for the change in percentage PD-L1 + endothelial cells (CD31 + ) (D) and percentage PD-L1 + neutrophils (Ly6G + ) (E) . A dotted line is provided to indicate median frequency of non-specific antibody binding typically detected using gating strategy during analysis, which was 2.75% ± 1.77% CD31 + PD-L1 + (D) and 2.29 ± 0.50% Ly6G + PD-L1 + (E) , respectively. The presence of a significant difference between groups was established at * p < 0.05 with a Mann–Whittney U test.
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Jackson Laboratory ve cadherin cdh5 cre mice
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Adheren Inc ve cadherin
HFPF disrupts <t>VE-cadherin-mediated</t> adherens junctions (A) Immunostaining of VE-cadherin (green) and phalloidin (red) after 24 h HFPF treatment. Scale bars, 100 μm. (B) Western blot analysis of VE-cadherin expression. (C) Fractionation analysis shows membranous and cytosolic VE-cadherin levels. Na + /K + -ATPase and GAPDH served as loading controls. Data means SEM. ∗ p < 0.05 and ∗∗ p < 0.01.
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Image Search Results


Description (A) and characterization of endothelial cell ( ec PD-L1 −/− ) (B, D) or neutrophil ( pmn PD-L1 −/− ) (C, E) restricted constitutive PD-L1 gene-deficient mice. Taconic Knockout Repository [mouse TF0103 (MGI:1926446); Taconic Biosciences Inc., Germantown, NY], CD274/PD-L1 conditional knockout mouse. PD-L1 gene exons 1 to 4 are shown as green boxes and loxP sites flanking exon 2 are depicted as red triangles (A) . Homozygous PD-L1 flox/flox were subsequently crossed to either VE-Cadherin‐Cre (B6.FVB-Tg[Cdh5-cre]7Mlia/J; Strain #:006137; RRID: IMSR_JAX:006137) or the S100a8-Cre (B6.Cg-Tg[S100a8-cre,-EGFP]1IIw/J; Strain #:021614; RRID: IMSR_JAX:021614) mice, obtained from Jackson Labs, to produce either mice homozygous for both the flox PD-L1 and specific cell-lineage Cre promoter genes or mice that were heterozygous for one or both genes that served as “Controls”. Gating strategy and typical flow cytogram/dot plot of select cell-lineage restricted PD-L1 expression [either CD31 and PD-L1 (B) or Ly6G and PD-L1 (C) ] for various breeding outcomes from respective Cre-Lox matings for PD-L1 flox/flox animals with VE-Cadherin‐Cre (B) or PD-L1 flox/flox animals with S100a8-Cre (C) . Summary data for the change in percentage PD-L1 + endothelial cells (CD31 + ) (D) and percentage PD-L1 + neutrophils (Ly6G + ) (E) . A dotted line is provided to indicate median frequency of non-specific antibody binding typically detected using gating strategy during analysis, which was 2.75% ± 1.77% CD31 + PD-L1 + (D) and 2.29 ± 0.50% Ly6G + PD-L1 + (E) , respectively. The presence of a significant difference between groups was established at * p < 0.05 with a Mann–Whittney U test.

Journal: Frontiers in Immunology

Article Title: Endothelial cell, but not neutrophil, programmed cell death receptor-ligand 1 loss has a morbid impact on experimental murine shock/sepsis-induced lung injury

doi: 10.3389/fimmu.2026.1816915

Figure Lengend Snippet: Description (A) and characterization of endothelial cell ( ec PD-L1 −/− ) (B, D) or neutrophil ( pmn PD-L1 −/− ) (C, E) restricted constitutive PD-L1 gene-deficient mice. Taconic Knockout Repository [mouse TF0103 (MGI:1926446); Taconic Biosciences Inc., Germantown, NY], CD274/PD-L1 conditional knockout mouse. PD-L1 gene exons 1 to 4 are shown as green boxes and loxP sites flanking exon 2 are depicted as red triangles (A) . Homozygous PD-L1 flox/flox were subsequently crossed to either VE-Cadherin‐Cre (B6.FVB-Tg[Cdh5-cre]7Mlia/J; Strain #:006137; RRID: IMSR_JAX:006137) or the S100a8-Cre (B6.Cg-Tg[S100a8-cre,-EGFP]1IIw/J; Strain #:021614; RRID: IMSR_JAX:021614) mice, obtained from Jackson Labs, to produce either mice homozygous for both the flox PD-L1 and specific cell-lineage Cre promoter genes or mice that were heterozygous for one or both genes that served as “Controls”. Gating strategy and typical flow cytogram/dot plot of select cell-lineage restricted PD-L1 expression [either CD31 and PD-L1 (B) or Ly6G and PD-L1 (C) ] for various breeding outcomes from respective Cre-Lox matings for PD-L1 flox/flox animals with VE-Cadherin‐Cre (B) or PD-L1 flox/flox animals with S100a8-Cre (C) . Summary data for the change in percentage PD-L1 + endothelial cells (CD31 + ) (D) and percentage PD-L1 + neutrophils (Ly6G + ) (E) . A dotted line is provided to indicate median frequency of non-specific antibody binding typically detected using gating strategy during analysis, which was 2.75% ± 1.77% CD31 + PD-L1 + (D) and 2.29 ± 0.50% Ly6G + PD-L1 + (E) , respectively. The presence of a significant difference between groups was established at * p < 0.05 with a Mann–Whittney U test.

Article Snippet: The VE-Cadherin‐Cre (Strain #:006137; RRID: IMSR_JAX:006137) and the S100a8-Cre (Strain #:021614; RRID: IMSR_JAX:021614) breeder mouse strains were also obtained from The Jackson Laboratory (see ).

Techniques: Knock-Out, Expressing, Binding Assay

HFPF disrupts VE-cadherin-mediated adherens junctions (A) Immunostaining of VE-cadherin (green) and phalloidin (red) after 24 h HFPF treatment. Scale bars, 100 μm. (B) Western blot analysis of VE-cadherin expression. (C) Fractionation analysis shows membranous and cytosolic VE-cadherin levels. Na + /K + -ATPase and GAPDH served as loading controls. Data means SEM. ∗ p < 0.05 and ∗∗ p < 0.01.

Journal: iScience

Article Title: Heart failure pleural fluid impairs endothelial barrier through miR 501-3p mediated ZO 1 remodeling

doi: 10.1016/j.isci.2026.115549

Figure Lengend Snippet: HFPF disrupts VE-cadherin-mediated adherens junctions (A) Immunostaining of VE-cadherin (green) and phalloidin (red) after 24 h HFPF treatment. Scale bars, 100 μm. (B) Western blot analysis of VE-cadherin expression. (C) Fractionation analysis shows membranous and cytosolic VE-cadherin levels. Na + /K + -ATPase and GAPDH served as loading controls. Data means SEM. ∗ p < 0.05 and ∗∗ p < 0.01.

Article Snippet: Adheren junctions modulate cell adhesion via cadherins, and VE-cadherin is one of the major cadherins in endothelial cells.

Techniques: Immunostaining, Western Blot, Expressing, Fractionation