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huvecs viability  (Dojindo Labs)


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    Dojindo Labs huvecs viability
    FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated <t>HUVECs</t> treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. <t>(D)</t> <t>CCK-8</t> assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.
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    Images

    1) Product Images from "Lenvatinib improves anti-PD-1 therapeutic efficacy by promoting vascular normalization via the NRP-1-PDGFRβ complex in hepatocellular carcinoma."

    Article Title: Lenvatinib improves anti-PD-1 therapeutic efficacy by promoting vascular normalization via the NRP-1-PDGFRβ complex in hepatocellular carcinoma.

    Journal: Frontiers in immunology

    doi: 10.3389/fimmu.2023.1212577

    FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (D) CCK-8 assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.
    Figure Legend Snippet: FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (D) CCK-8 assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.

    Techniques Used: Concentration Assay, Permeability, Western Blot, Phospho-proteomics, Expressing, Staining, CCK-8 Assay, Transwell Migration Assay, Labeling, Cell Culture, Microscopy

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    CCK-8 Assay:

    Article Title: Lenvatinib improves anti-PD-1 therapeutic efficacy by promoting vascular normalization via the NRP-1-PDGFRβ complex in hepatocellular carcinoma
    Article Snippet: The samples were ultimately eluted 1×SDS-PAGE (Beyotime) sample buffer and further assessed by Western blot analysis. .. HUVECs viability was determined using the cell counting kit-8 (CCK-8) cell viability assay (Dojindo Laboratories, Kumamoto, Japan). ..

    Article Title: MicroRNA-195-3p as a potential regulator of hypoxic injury in HUVECs
    Article Snippet: .. HUVECS viability was assessed by Cell Counting Kit-8 (CCK-8, Dojindo, Japan) assay as described previously. ..

    Article Title: Maternal Supplementation of Low Dose Fluoride Alleviates Adverse Perinatal Outcomes Following Exposure to Intrauterine Inflammation
    Article Snippet: .. HUVECs viability was determined with Cell Counting Kit-8 Assay Kit (CKK-8) (Dojindo Molecular Technologies, Inc., Rockville, Maryland, USA). .. The absorbance was measured with a microplate reader (BMG LABTECH, Inc., Cary, NC, USA) at a wavelength of 450 nm.

    Article Title: Lenvatinib improves anti-PD-1 therapeutic efficacy by promoting vascular normalization via the NRP-1-PDGFRβ complex in hepatocellular carcinoma.
    Article Snippet: The samples were ultimately eluted 1×SDS-PAGE (Beyotime) sample buffer and further assessed by Western blot analysis. .. HUVECs viability was determined using the cell counting kit-8 (CCK-8) cell viability assay (Dojindo Laboratories, Kumamoto, Japan). ..

    Article Title: Liraglutide prevents high glucose induced HUVECs dysfunction via inhibition of PINK1/Parkin-dependent mitophagy.
    Article Snippet: The images (magnification × 100) were captured by a computerized fluorescence microscope (IX71, Olympus). .. The HUVECs viability was measured with a Cell Counting Kit-8 (CCK-8, Dojindo, Japan) according to the manufacturer’s instruction. ..

    Article Title: Maternal Supplementation of Low Dose Fluoride Alleviates Adverse Perinatal Outcomes Following Exposure to Intrauterine Inflammation.
    Article Snippet: .. HUVECs viability was determined with Cell Counting Kit-8 Assay Kit (CKK-8) (Dojindo Molecular Technologies, Inc., Rockville, Maryland, USA). .. The absorbance was measured with a microplate reader (BMG LABTECH, Inc., Cary, NC, USA) at a wavelength of 450 nm.

    Viability Assay:

    Article Title: Lenvatinib improves anti-PD-1 therapeutic efficacy by promoting vascular normalization via the NRP-1-PDGFRβ complex in hepatocellular carcinoma
    Article Snippet: The samples were ultimately eluted 1×SDS-PAGE (Beyotime) sample buffer and further assessed by Western blot analysis. .. HUVECs viability was determined using the cell counting kit-8 (CCK-8) cell viability assay (Dojindo Laboratories, Kumamoto, Japan). ..

    Article Title: Lenvatinib improves anti-PD-1 therapeutic efficacy by promoting vascular normalization via the NRP-1-PDGFRβ complex in hepatocellular carcinoma.
    Article Snippet: The samples were ultimately eluted 1×SDS-PAGE (Beyotime) sample buffer and further assessed by Western blot analysis. .. HUVECs viability was determined using the cell counting kit-8 (CCK-8) cell viability assay (Dojindo Laboratories, Kumamoto, Japan). ..



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    FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated <t>HUVECs</t> treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. <t>(D)</t> <t>CCK-8</t> assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.
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    FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated <t>HUVECs</t> treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. <t>(D)</t> <t>CCK-8</t> assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.
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    FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated <t>HUVECs</t> treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. <t>(D)</t> <t>CCK-8</t> assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.
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    FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated <t>HUVECs</t> treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. <t>(D)</t> <t>CCK-8</t> assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.
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    FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated <t>HUVECs</t> treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. <t>(D)</t> <t>CCK-8</t> assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.
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    FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated <t>HUVECs</t> treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. <t>(D)</t> <t>CCK-8</t> assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.
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    Effect of paeoniflorin (PF) on HUVECs. (A) PF chemical structure. (B) Evaluation of <t>HUVEC</t> <t>viability</t> using CCK-8 assay after exposure to differing concentrations of PF for 24 h. (C) Evaluation of HUVEC viability using CCK-8 assay after stimulation to different concentrations of TBHP for 24 h. (D) Representative images demonstrating cell morphology alterations in PF and TBHP co-treatment in HUVECs (scan bar, 100 μm). (E) Evaluation of HUVEC viability using CCK-8 assay after PF and TBHP co-treatment in HUVECs. Data: mean ± SD, * p < 0.05 and ** p < 0.01. n = 3.
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    Image Search Results


    FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (D) CCK-8 assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.

    Journal: Frontiers in immunology

    Article Title: Lenvatinib improves anti-PD-1 therapeutic efficacy by promoting vascular normalization via the NRP-1-PDGFRβ complex in hepatocellular carcinoma.

    doi: 10.3389/fimmu.2023.1212577

    Figure Lengend Snippet: FIGURE 3 The concentration-escalation treatment with lenvatinib showed different phenotypes of vascular permeability and interaction with pericytes. (A) The permeability of the endothelial monolayer was assessed by the passage of Evans blue (EB)/albumin through the upper endothelial monolayer in the lower chamber (n=3 separate experiments). (B) Western blot analysis of the phosphorylation of VE-cadherin and VEGFR2 and total expression of VE-cadherin and VEGFR2 in the indicated HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (C) Representative IF staining images of VE-cadherin (green) in HUVECs treated with lenvatinib at different concentrations for 2 h, followed by stimulation with 60 ng/ml VEGF for 1 hour. (D) CCK-8 assay showing the proliferation of the indicated HBVPs with different treatments at different time points. (E) The OD450 value of the indicated HBVPs after different treatments for 72 h. (F) Representative images of the indicated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (G) Statistical graphs of migrated HBVPs assessed by the Transwell migration assay after different treatments for 72 h. (H, I) Fluorescently-labeled pericytes (green) were plated together with red-labeled endothelial cells (ECs) onto Matrigel at a 4:1 (EC: pericyte) ratio, cultured for 24 h (H) and 48 h (I), and the resulting vessel-like structures were analyzed by fluorescent microscopy. The error bars represent the mean ± SD. *P < 0.05; **P < 0.01; *** P < 0.001; ****P < 0.0001; ns indicates non-significant.

    Article Snippet: HUVECs viability was determined using the cell counting kit-8 (CCK-8) cell viability assay (Dojindo Laboratories, Kumamoto, Japan).

    Techniques: Concentration Assay, Permeability, Western Blot, Phospho-proteomics, Expressing, Staining, CCK-8 Assay, Transwell Migration Assay, Labeling, Cell Culture, Microscopy

    Effect of paeoniflorin (PF) on HUVECs. (A) PF chemical structure. (B) Evaluation of HUVEC viability using CCK-8 assay after exposure to differing concentrations of PF for 24 h. (C) Evaluation of HUVEC viability using CCK-8 assay after stimulation to different concentrations of TBHP for 24 h. (D) Representative images demonstrating cell morphology alterations in PF and TBHP co-treatment in HUVECs (scan bar, 100 μm). (E) Evaluation of HUVEC viability using CCK-8 assay after PF and TBHP co-treatment in HUVECs. Data: mean ± SD, * p < 0.05 and ** p < 0.01. n = 3.

    Journal: Frontiers in Pharmacology

    Article Title: Paeoniflorin Suppresses TBHP-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells via the Nrf2/HO-1 Signaling Pathway and Improves Skin Flap Survival

    doi: 10.3389/fphar.2021.735530

    Figure Lengend Snippet: Effect of paeoniflorin (PF) on HUVECs. (A) PF chemical structure. (B) Evaluation of HUVEC viability using CCK-8 assay after exposure to differing concentrations of PF for 24 h. (C) Evaluation of HUVEC viability using CCK-8 assay after stimulation to different concentrations of TBHP for 24 h. (D) Representative images demonstrating cell morphology alterations in PF and TBHP co-treatment in HUVECs (scan bar, 100 μm). (E) Evaluation of HUVEC viability using CCK-8 assay after PF and TBHP co-treatment in HUVECs. Data: mean ± SD, * p < 0.05 and ** p < 0.01. n = 3.

    Article Snippet: HUVEC viability were evaluated with the Cell Counting Kit-8 (CCK-8) assay (MedChemExpress LLC; Monmouth Junction, NJ, United States), following operational guidelines.

    Techniques: CCK-8 Assay