ve cadherin  (Proteintech)

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: circIdh2 attenuated TGF‐ β 1–induced EndMT changes in rEPCs. rEPCs were treated with or without TGF‐ β 1 (5 ng/mL) for 7 days, and then transfected with PCDH‐NC or PCDH‐circIdh2. (A) qRT‐PCR analysis of circIdh2 expression after transfection for 24 h. (B) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin) after transfection for 48 h. (C) Transwell assay was performed to assess cell migration after transfection for 24 h. (D) Representative scratch wound healing images at 0, 24, and 48 h. Scale bars, 200 μ m. (E) Quantification of relative wound width (% of PCDH‐NC at 0 h). Data are mean ± SD; n = 3 independent biological experiments; one‐way ANOVA; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The primary antibodies used were as follows: VE‐cadherin (1:1000, #27956‐1‐AP, Proteintech, Wuhan, China), vimentin (1:1000, #ap2739b, Abcepta, Jiangsu, China), N‐cadherin (1:5000, #22018‐1‐AP, Proteintech), FLAG (1:2000, #20543‐1‐AP, Proteintech), and GAPDH (1:50000, #60004‐1‐Ig, Proteintech).

Techniques: Transfection, Quantitative RT-PCR, Analysis, Expressing, Western Blot, Transwell Assay, Migration

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: Knockdown of circIdh2 promoted EndMT changes in rEPCs. rEPCs were transfected with si‐NC or siRNAs targeting circIdh2. (A) qRT‐PCR analysis of circIdh2 expression after transfection for 24 h. (B) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin) after transfection for 48 h. (C) Cell migration was assessed using a Transwell assay after transfection for 24 h. (D) Representative scratch wound healing images were obtained at 0, 24, and 48 h. Scale bars, 200 μ m. (E) Quantification of relative wound width (% of si‐NC at 0 h). Data are mean ± SD; n = 3 independent biological experiments; Student′s t ‐test was used for two‐group comparisons and one‐way ANOVA for multiple‐group comparisons; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The primary antibodies used were as follows: VE‐cadherin (1:1000, #27956‐1‐AP, Proteintech, Wuhan, China), vimentin (1:1000, #ap2739b, Abcepta, Jiangsu, China), N‐cadherin (1:5000, #22018‐1‐AP, Proteintech), FLAG (1:2000, #20543‐1‐AP, Proteintech), and GAPDH (1:50000, #60004‐1‐Ig, Proteintech).

Techniques: Knockdown, Transfection, Quantitative RT-PCR, Analysis, Expressing, Western Blot, Migration, Transwell Assay

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: The FLAG‐tagged circIdh2 construct affected EndMT‐related markers and cell migration in rEPCs. rEPCs were transfected with PCDH‐NC or PCDH‐flag‐circIdh2. (A) qRT‐PCR analysis of circIdh2 expression after transfection for 24 h. (B) Western blot analysis of FLAG expression after transfection for 48 h. (C) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin) after transfection for 48 h. (D) Cell migration was examined by Transwell assay after transfection for 24 h. (E) Representative images from the scratch wound healing assay at 0, 24, and 48 h. Scale bar, 200 μ m. (F) Quantification of relative wound width (% of PCDH‐NC at 0 h). Data are mean ± SD; n = 3 independent biological experiments; unpaired Student′s t ‐test; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The primary antibodies used were as follows: VE‐cadherin (1:1000, #27956‐1‐AP, Proteintech, Wuhan, China), vimentin (1:1000, #ap2739b, Abcepta, Jiangsu, China), N‐cadherin (1:5000, #22018‐1‐AP, Proteintech), FLAG (1:2000, #20543‐1‐AP, Proteintech), and GAPDH (1:50000, #60004‐1‐Ig, Proteintech).

Techniques: Construct, Migration, Transfection, Quantitative RT-PCR, Analysis, Expressing, Western Blot, Transwell Assay, Wound Healing Assay

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: The circIdh2 mutant did not reproduce the effects of wild‐type circIdh2 on EndMT‐related markers and cell migration. rEPCs were transfected with PCDH‐NC, PCDH‐circIdh2, or PCDH‐circIdh2‐mut. (A) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin) after transfection for 48 h. (B) Cell migration was assessed using a Transwell assay after transfection for 24 h. (C) Representative scratch wound healing images at 0, 24, and 48 h, with quantification of relative wound width (% of PCDH‐NC at 0 h). Scale bar, 200 μ m. Data are mean ± SD; n = 3 independent biological experiments; one‐way ANOVA; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The primary antibodies used were as follows: VE‐cadherin (1:1000, #27956‐1‐AP, Proteintech, Wuhan, China), vimentin (1:1000, #ap2739b, Abcepta, Jiangsu, China), N‐cadherin (1:5000, #22018‐1‐AP, Proteintech), FLAG (1:2000, #20543‐1‐AP, Proteintech), and GAPDH (1:50000, #60004‐1‐Ig, Proteintech).

Techniques: Mutagenesis, Migration, Transfection, Western Blot, Analysis, Transwell Assay

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: AAV‐mediated delivery of circIdh2 or circIdh2‐aa attenuated myocardial fibrosis and EndMT‐related marker changes in vivo. (A) HE staining of myocardial infarction tissues from the sham, model, circIdh2‐AAV, and circIdh2‐aa‐AAV groups. (B) Masson staining of MI tissues. (C) IF detection and quantification of fibrotic markers (Collagen I and TGF‐ β ) in myocardial tissues. Scale bars, 100 μ m. (D) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin). Data are mean ± SD; n = 3 rats per group; one‐way ANOVA; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The primary antibodies used were as follows: VE‐cadherin (1:1000, #27956‐1‐AP, Proteintech, Wuhan, China), vimentin (1:1000, #ap2739b, Abcepta, Jiangsu, China), N‐cadherin (1:5000, #22018‐1‐AP, Proteintech), FLAG (1:2000, #20543‐1‐AP, Proteintech), and GAPDH (1:50000, #60004‐1‐Ig, Proteintech).

Techniques: Marker, In Vivo, H&E Stain, Staining, Western Blot, Analysis

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