Journal: Frontiers in Cardiovascular Medicine

Article Title: A refined protocol for the isolation and monoculture of primary mouse renal peritubular endothelial cells

doi: 10.3389/fcvm.2023.1114726

Figure Lengend Snippet: Reagents and resources list for MRPEC isolation.

Article Snippet: CD144 (VE-cadherin) antibody, APC, REAfinity , Recombinant human IgG1; Human anti-Mouse Monoclonal (REA225) , 1:50 , Miltenyi Biotec , 130-102-738.

Techniques: Isolation, Immunofluorescence, Staining, Flow Cytometry, Recombinant, Concentration Assay, Control, Sterility, Membrane, Cell Culture, Centrifugation, Polymer, Blocking Assay, Purification, Binding Assay, Clinical Proteomics

Journal: Frontiers in physiology

Article Title: Microvesicles Derived from Indoxyl Sulfate Treated Endothelial Cells Induce Endothelial Progenitor Cells Dysfunction.

doi: 10.3389/fphys.2017.00666

Figure Lengend Snippet: FIGURE 1 | Indoxyl sulfate (IS) induces activation in human umbilical vein endothelial cells (HUVECs). HUVECs treated with IS (256 µg/ml) for 24 h showed significant increases in markers of oxidative stress and apoptosis. The expression was quantified by changes in the mean fluorescent intensity (MFI) of (A) hydroethidine (HE) and (B) annexin V. In addition, (C) IS induced significantly elevated expression of ICAM-1, VE-cadherin, and VCAM-1, but not PECAM-1. Data are the means ± SEM of five independent experiments. *p = 0.004 vs. untreated HUVECs; **p = 0.045 vs. untreated HUVECs; and #p ≤0.001 vs. untreated HUVECs.

Article Snippet: Next, VE-cadherin (FITC rabbit anti human CD144, AbD Serotec, UK), PECAM-1 (PE-labeled monoclonal antiCD31, Caltag Laboratories, Burlingame, CA, USA), ICAM-1 (PE mouse anti human CD54, Invitrogen), and VCAM-1 (PE Mouse Anti-Human CD106, BD Pharmingen) antibodies were used to assess the expression in the experimental conditions.

Techniques: Activation Assay, Expressing

Journal: Frontiers in physiology

Article Title: Microvesicles Derived from Indoxyl Sulfate Treated Endothelial Cells Induce Endothelial Progenitor Cells Dysfunction.

doi: 10.3389/fphys.2017.00666

Figure Lengend Snippet: FIGURE 3 | Indoxyl sulfate (IS) modulates the expression of adhesion molecules and annexin V in microvesicles (MV). MV (MV/µl) derived from indoxyl sulfate-treated HUVECs (IsEMV) showed a significant increase in annexin V and adhesion molecules, such as PECAM-1, VE-cadherin, and ICAM-1, but not VCAM-1. Results are the mean ± SEM of five independent experiments. *p < 0.001 vs. MV derived from untreated HUVECs (EMV); **p = 0.002 vs. EMV and #p = 0.014 vs. EMV.

Article Snippet: Next, VE-cadherin (FITC rabbit anti human CD144, AbD Serotec, UK), PECAM-1 (PE-labeled monoclonal antiCD31, Caltag Laboratories, Burlingame, CA, USA), ICAM-1 (PE mouse anti human CD54, Invitrogen), and VCAM-1 (PE Mouse Anti-Human CD106, BD Pharmingen) antibodies were used to assess the expression in the experimental conditions.

Techniques: Expressing, Derivative Assay

Journal: Frontiers in Pharmacology

Article Title: Butylphthalide Inhibits Autophagy and Promotes Multiterritory Perforator Flap Survival

doi: 10.3389/fphar.2020.612932

Figure Lengend Snippet: NBP improves angiogenesis in multiterritory perforator flap. (A) and (B) IHC of VEGF and CDH5 in the ischemic flap of the control and NBP-treated rats. (C) and (D) Optical density values of VEGF and CDH5. (E) Western blotting of MMP9, VEGF, and CDH5 in control and NBP-treated groups. (F) Optical density values of MMP9, VEGF, and CDH5 from western blot. Gels were run under similar experimental conditions and cropped edited only for clarity. Values are shown as mean ± SEM, n = 6 per group. * p < 0.05 and ** p < 0.01 vs. control group.

Article Snippet: The primary antibody against CDH5 was acquired from Boster Biological Technology (A02632-2; Hangzhou, China).

Techniques: Control, Western Blot

Journal: Frontiers in Pharmacology

Article Title: Butylphthalide Inhibits Autophagy and Promotes Multiterritory Perforator Flap Survival

doi: 10.3389/fphar.2020.612932

Figure Lengend Snippet: Rapamycin reverses effects of NBP on angiogenesis, oxidative stress, and apoptosis in multiterritory perforator flap. (A) Autophagosomes (LC3, red) in cells in the control, NBP, NBP + rapamycin, and rapamycin groups. Nuclei are counterstained with DAPI (blue) (scale bar, 20 μm). (B) Digital images of the control, NBP, NBP + rapamycin, and rapamycin groups on POD 7. (C) LDBF in each group on POD 7. (D) Percentage of survival area on POD 7. (E) Percentage of the signal intensity of blood flow within the flap in each group. (F) LC3 positive cells in each group. (G) Autophagy-related protein expression (LC3, CTSD, Beclin1, and SQSTM1/p62) and angiogenesis-related proteins (VEGF, MMP9, and CDH5). (H) Optical density of LC3, CTSD, Beclin1, SQSTM1/p62, VEGF, MMP9, and CDH5 in each group. (L) Apoptosis-related protein expression (CYC, Bax, and CASP3) and oxidative stress-related protein expression (SOD1, HO1, and eNOS) in each group. (M) Optical density of CYC, Bax, CASP3, SOD1, HO1, and eNOS expressions in each group. Gels were run under similar experimental conditions and edited only for clarity. Values are shown as mean ± SEM, n = 6 per group. * p < 0.05 and ** p < 0.01 vs. control group; # p < 0.05 and ## p < 0.01 vs. NBP group.

Article Snippet: The primary antibody against CDH5 was acquired from Boster Biological Technology (A02632-2; Hangzhou, China).

Techniques: Control, Expressing