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ecis model z theta applied biophysics  (Applied BioPhysics)


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    Applied BioPhysics ecis model z theta applied biophysics
    S1 and plasma from PCS patients influence ROS production, impair NO availability, and disrupt barrier integrity in HRECs, effects improved by belzutifan. (A) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA (n = 3 independent experiments). (B) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 4 h, and mitochondrial ROS production was measured by flow cytometric analysis using MitoSox Red (n = 4 independent experiments). (C, D) HRECs were mock-treated (control), stimulated with S1 (100 ng/mL) or CoCl 2 (100 µM), and treated with belzutifan (50 nM) for 72 h. Immunofluorescence staining was performed for F-actin (C, red ) and VE-cadherin (D, green ) , with nuclei counterstained with DAPI (blue). Images (left) were acquired at 20× magnification, and scale bars represent 100 µm. Graphs (right) illustrate the percentage of positive cells (C) and the corrected total cell fluorescence (CTCF) (D) (n = 3 independent experiments). (E) HRECs were cultured at confluence on <t>ECIS</t> electrodes and then stimulated with 100 ng/mL S1 or left untreated in the presence or absence of 50 nM belzutifan for 0–72 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons (n = 3 independent experiments). (F) HRECs were treated with 2% plasma from healthy individuals (HC, n=8) or PCS patients (n=13) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA. (G) Mitochondrial ROS production in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h, measured by flow cytometric analysis using MitoSox Red. (H) Total NO levels in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h and 24 h, measured using a fluorometric assay for total nitrite/nitrate levels. (I) HRECs were cultured at confluence on ECIS electrodes and exposed to 2% plasma from HC or PCS patients in the presence or absence of 50 nM belzutifan for 0–48 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons. Data are represented as means ± SD. Each dot represents one independent experiment for S1 studies or one individual donor for plasma studies. A p-value of <0.05 was considered statistically significant. P-values were determined by two-way ANOVA followed by Tukey’s post hoc test (A, E, F, I) , Mann–Whitney U test (B) , one-way ANOVA followed by Tukey’s post hoc test (C, D) , Student’s t-test (G) , and Kruskal–Wallis test followed by Dunn’s post hoc test (H) . .
    Ecis Model Z Theta Applied Biophysics, supplied by Applied BioPhysics, used in various techniques. Bioz Stars score: 96/100, based on 636 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ecis+model+z+theta+applied+biophysics/ECIS+Z+Theta/pmc13006635-135-15-18
    Average 96 stars, based on 636 article reviews
    ecis model z theta applied biophysics - by Bioz Stars, 2026-09
    96/100 stars

    Images

    1) Product Images from "SARS−CoV−2 spike S1-mediated HIF−2α activation in retinal endothelial cells suggests a mechanism contributing to post−COVID endothelial dysfunction"

    Article Title: SARS−CoV−2 spike S1-mediated HIF−2α activation in retinal endothelial cells suggests a mechanism contributing to post−COVID endothelial dysfunction

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2026.1770758

    S1 and plasma from PCS patients influence ROS production, impair NO availability, and disrupt barrier integrity in HRECs, effects improved by belzutifan. (A) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA (n = 3 independent experiments). (B) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 4 h, and mitochondrial ROS production was measured by flow cytometric analysis using MitoSox Red (n = 4 independent experiments). (C, D) HRECs were mock-treated (control), stimulated with S1 (100 ng/mL) or CoCl 2 (100 µM), and treated with belzutifan (50 nM) for 72 h. Immunofluorescence staining was performed for F-actin (C, red ) and VE-cadherin (D, green ) , with nuclei counterstained with DAPI (blue). Images (left) were acquired at 20× magnification, and scale bars represent 100 µm. Graphs (right) illustrate the percentage of positive cells (C) and the corrected total cell fluorescence (CTCF) (D) (n = 3 independent experiments). (E) HRECs were cultured at confluence on ECIS electrodes and then stimulated with 100 ng/mL S1 or left untreated in the presence or absence of 50 nM belzutifan for 0–72 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons (n = 3 independent experiments). (F) HRECs were treated with 2% plasma from healthy individuals (HC, n=8) or PCS patients (n=13) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA. (G) Mitochondrial ROS production in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h, measured by flow cytometric analysis using MitoSox Red. (H) Total NO levels in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h and 24 h, measured using a fluorometric assay for total nitrite/nitrate levels. (I) HRECs were cultured at confluence on ECIS electrodes and exposed to 2% plasma from HC or PCS patients in the presence or absence of 50 nM belzutifan for 0–48 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons. Data are represented as means ± SD. Each dot represents one independent experiment for S1 studies or one individual donor for plasma studies. A p-value of <0.05 was considered statistically significant. P-values were determined by two-way ANOVA followed by Tukey’s post hoc test (A, E, F, I) , Mann–Whitney U test (B) , one-way ANOVA followed by Tukey’s post hoc test (C, D) , Student’s t-test (G) , and Kruskal–Wallis test followed by Dunn’s post hoc test (H) . .
    Figure Legend Snippet: S1 and plasma from PCS patients influence ROS production, impair NO availability, and disrupt barrier integrity in HRECs, effects improved by belzutifan. (A) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA (n = 3 independent experiments). (B) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 4 h, and mitochondrial ROS production was measured by flow cytometric analysis using MitoSox Red (n = 4 independent experiments). (C, D) HRECs were mock-treated (control), stimulated with S1 (100 ng/mL) or CoCl 2 (100 µM), and treated with belzutifan (50 nM) for 72 h. Immunofluorescence staining was performed for F-actin (C, red ) and VE-cadherin (D, green ) , with nuclei counterstained with DAPI (blue). Images (left) were acquired at 20× magnification, and scale bars represent 100 µm. Graphs (right) illustrate the percentage of positive cells (C) and the corrected total cell fluorescence (CTCF) (D) (n = 3 independent experiments). (E) HRECs were cultured at confluence on ECIS electrodes and then stimulated with 100 ng/mL S1 or left untreated in the presence or absence of 50 nM belzutifan for 0–72 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons (n = 3 independent experiments). (F) HRECs were treated with 2% plasma from healthy individuals (HC, n=8) or PCS patients (n=13) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA. (G) Mitochondrial ROS production in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h, measured by flow cytometric analysis using MitoSox Red. (H) Total NO levels in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h and 24 h, measured using a fluorometric assay for total nitrite/nitrate levels. (I) HRECs were cultured at confluence on ECIS electrodes and exposed to 2% plasma from HC or PCS patients in the presence or absence of 50 nM belzutifan for 0–48 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons. Data are represented as means ± SD. Each dot represents one independent experiment for S1 studies or one individual donor for plasma studies. A p-value of <0.05 was considered statistically significant. P-values were determined by two-way ANOVA followed by Tukey’s post hoc test (A, E, F, I) , Mann–Whitney U test (B) , one-way ANOVA followed by Tukey’s post hoc test (C, D) , Student’s t-test (G) , and Kruskal–Wallis test followed by Dunn’s post hoc test (H) . .

    Techniques Used: Clinical Proteomics, Control, Immunofluorescence, Staining, Fluorescence, Cell Culture, MANN-WHITNEY

    Related Articles

    Electric Cell-substrate Impedance Sensing:

    Article Title: Inhibition of HIF-2α Pathway as a Potential Therapeutic Strategy for Endothelial Dysfunction in Post-COVID Syndrome
    Article Snippet: .. The barrier function of confluent endothelial cell monolayers was estimated using electric cell-substrate impedance sensing (ECIS) model Z-Theta (Applied Biophysics) as described [ ]. ..

    Article Title: SARS−CoV−2 spike S1-mediated HIF−2α activation in retinal endothelial cells suggests a mechanism contributing to post−COVID endothelial dysfunction
    Article Snippet: .. The barrier function of confluent endothelial cell monolayers was estimated using electric cell‐substrate impedance sensing (ECIS) model Z-Theta (Applied Biophysics) as described ( ). ..



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    S1 and plasma from PCS patients influence ROS production, impair NO availability, and disrupt barrier integrity in HRECs, effects improved by belzutifan. (A) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA (n = 3 independent experiments). (B) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 4 h, and mitochondrial ROS production was measured by flow cytometric analysis using MitoSox Red (n = 4 independent experiments). (C, D) HRECs were mock-treated (control), stimulated with S1 (100 ng/mL) or CoCl 2 (100 µM), and treated with belzutifan (50 nM) for 72 h. Immunofluorescence staining was performed for F-actin (C, red ) and VE-cadherin (D, green ) , with nuclei counterstained with DAPI (blue). Images (left) were acquired at 20× magnification, and scale bars represent 100 µm. Graphs (right) illustrate the percentage of positive cells (C) and the corrected total cell fluorescence (CTCF) (D) (n = 3 independent experiments). (E) HRECs were cultured at confluence on <t>ECIS</t> electrodes and then stimulated with 100 ng/mL S1 or left untreated in the presence or absence of 50 nM belzutifan for 0–72 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons (n = 3 independent experiments). (F) HRECs were treated with 2% plasma from healthy individuals (HC, n=8) or PCS patients (n=13) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA. (G) Mitochondrial ROS production in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h, measured by flow cytometric analysis using MitoSox Red. (H) Total NO levels in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h and 24 h, measured using a fluorometric assay for total nitrite/nitrate levels. (I) HRECs were cultured at confluence on ECIS electrodes and exposed to 2% plasma from HC or PCS patients in the presence or absence of 50 nM belzutifan for 0–48 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons. Data are represented as means ± SD. Each dot represents one independent experiment for S1 studies or one individual donor for plasma studies. A p-value of <0.05 was considered statistically significant. P-values were determined by two-way ANOVA followed by Tukey’s post hoc test (A, E, F, I) , Mann–Whitney U test (B) , one-way ANOVA followed by Tukey’s post hoc test (C, D) , Student’s t-test (G) , and Kruskal–Wallis test followed by Dunn’s post hoc test (H) . .
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    S1 and plasma from PCS patients influence ROS production, impair NO availability, and disrupt barrier integrity in HRECs, effects improved by belzutifan. (A) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA (n = 3 independent experiments). (B) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 4 h, and mitochondrial ROS production was measured by flow cytometric analysis using MitoSox Red (n = 4 independent experiments). (C, D) HRECs were mock-treated (control), stimulated with S1 (100 ng/mL) or CoCl 2 (100 µM), and treated with belzutifan (50 nM) for 72 h. Immunofluorescence staining was performed for F-actin (C, red ) and VE-cadherin (D, green ) , with nuclei counterstained with DAPI (blue). Images (left) were acquired at 20× magnification, and scale bars represent 100 µm. Graphs (right) illustrate the percentage of positive cells (C) and the corrected total cell fluorescence (CTCF) (D) (n = 3 independent experiments). (E) HRECs were cultured at confluence on ECIS electrodes and then stimulated with 100 ng/mL S1 or left untreated in the presence or absence of 50 nM belzutifan for 0–72 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons (n = 3 independent experiments). (F) HRECs were treated with 2% plasma from healthy individuals (HC, n=8) or PCS patients (n=13) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA. (G) Mitochondrial ROS production in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h, measured by flow cytometric analysis using MitoSox Red. (H) Total NO levels in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h and 24 h, measured using a fluorometric assay for total nitrite/nitrate levels. (I) HRECs were cultured at confluence on ECIS electrodes and exposed to 2% plasma from HC or PCS patients in the presence or absence of 50 nM belzutifan for 0–48 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons. Data are represented as means ± SD. Each dot represents one independent experiment for S1 studies or one individual donor for plasma studies. A p-value of <0.05 was considered statistically significant. P-values were determined by two-way ANOVA followed by Tukey’s post hoc test (A, E, F, I) , Mann–Whitney U test (B) , one-way ANOVA followed by Tukey’s post hoc test (C, D) , Student’s t-test (G) , and Kruskal–Wallis test followed by Dunn’s post hoc test (H) . .

    Journal: Frontiers in Immunology

    Article Title: SARS−CoV−2 spike S1-mediated HIF−2α activation in retinal endothelial cells suggests a mechanism contributing to post−COVID endothelial dysfunction

    doi: 10.3389/fimmu.2026.1770758

    Figure Lengend Snippet: S1 and plasma from PCS patients influence ROS production, impair NO availability, and disrupt barrier integrity in HRECs, effects improved by belzutifan. (A) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA (n = 3 independent experiments). (B) HRECs were mock-treated (control) or stimulated with S1 (100 ng/ml) for 4 h, and mitochondrial ROS production was measured by flow cytometric analysis using MitoSox Red (n = 4 independent experiments). (C, D) HRECs were mock-treated (control), stimulated with S1 (100 ng/mL) or CoCl 2 (100 µM), and treated with belzutifan (50 nM) for 72 h. Immunofluorescence staining was performed for F-actin (C, red ) and VE-cadherin (D, green ) , with nuclei counterstained with DAPI (blue). Images (left) were acquired at 20× magnification, and scale bars represent 100 µm. Graphs (right) illustrate the percentage of positive cells (C) and the corrected total cell fluorescence (CTCF) (D) (n = 3 independent experiments). (E) HRECs were cultured at confluence on ECIS electrodes and then stimulated with 100 ng/mL S1 or left untreated in the presence or absence of 50 nM belzutifan for 0–72 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons (n = 3 independent experiments). (F) HRECs were treated with 2% plasma from healthy individuals (HC, n=8) or PCS patients (n=13) for 0–6 h, and cellular ROS levels were measured using DCFDA/H 2 DCFDA. (G) Mitochondrial ROS production in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h, measured by flow cytometric analysis using MitoSox Red. (H) Total NO levels in HRECs exposed to 2% plasma from HC (n=8) or PCS patients (n=13) for 4 h and 24 h, measured using a fluorometric assay for total nitrite/nitrate levels. (I) HRECs were cultured at confluence on ECIS electrodes and exposed to 2% plasma from HC or PCS patients in the presence or absence of 50 nM belzutifan for 0–48 h. The loss of barrier integrity was determined by transendothelial electrical resistance (TEER). Values were normalized to time = 0 for easier comparisons. Data are represented as means ± SD. Each dot represents one independent experiment for S1 studies or one individual donor for plasma studies. A p-value of <0.05 was considered statistically significant. P-values were determined by two-way ANOVA followed by Tukey’s post hoc test (A, E, F, I) , Mann–Whitney U test (B) , one-way ANOVA followed by Tukey’s post hoc test (C, D) , Student’s t-test (G) , and Kruskal–Wallis test followed by Dunn’s post hoc test (H) . .

    Article Snippet: The barrier function of confluent endothelial cell monolayers was estimated using electric cell‐substrate impedance sensing (ECIS) model Z-Theta (Applied Biophysics) as described ( ).

    Techniques: Clinical Proteomics, Control, Immunofluorescence, Staining, Fluorescence, Cell Culture, MANN-WHITNEY

    Effect of aging on pulmonary microvascular endothelial cell (PMVEC) permeability under basal conditions. A) Monolayer resistance was assessed in PMVEC from young and aged mice by electric cell-substrate impedance sensing (ECIS). Compared to young, PMVEC from aged mice exhibited significantly decreased monolayer resistance 26 hours after seeding. B) Immunofluorescent (IF) staining of vascular endothelial (VE)-cadherin (RED) and local leak of NeutrAvidin (GREEN) was carried out in PMVEC monolayers from young and aged animals. PMVEC from young mice exhibited continuous VE-cadherin IF staining around the periphery of the cells, and this was associated with minimal leak. In contrast, PMVEC from aged mice exhibited discontinuous VE-cadherin IF staining (white arrows) and significantly increased avidin leak, with areas of leak colocalized directly at paracellular regions of VE-cadherin discontinuity. For ECIS experiments, n = 4; *p<0.05; Repeated measures two-way ANOVA. For NeutrAvidin Leak experiments, n = 3; ***p<0.001; Unpaired t-test. Scale bar = 100 μm.

    Journal: bioRxiv

    Article Title: The role of aging on endothelial cell-cell junctions and pulmonary microvascular permeability

    doi: 10.1101/2025.07.29.667420

    Figure Lengend Snippet: Effect of aging on pulmonary microvascular endothelial cell (PMVEC) permeability under basal conditions. A) Monolayer resistance was assessed in PMVEC from young and aged mice by electric cell-substrate impedance sensing (ECIS). Compared to young, PMVEC from aged mice exhibited significantly decreased monolayer resistance 26 hours after seeding. B) Immunofluorescent (IF) staining of vascular endothelial (VE)-cadherin (RED) and local leak of NeutrAvidin (GREEN) was carried out in PMVEC monolayers from young and aged animals. PMVEC from young mice exhibited continuous VE-cadherin IF staining around the periphery of the cells, and this was associated with minimal leak. In contrast, PMVEC from aged mice exhibited discontinuous VE-cadherin IF staining (white arrows) and significantly increased avidin leak, with areas of leak colocalized directly at paracellular regions of VE-cadherin discontinuity. For ECIS experiments, n = 4; *p<0.05; Repeated measures two-way ANOVA. For NeutrAvidin Leak experiments, n = 3; ***p<0.001; Unpaired t-test. Scale bar = 100 μm.

    Article Snippet: Cells were grown in complete DMEM, and resistance was continuously monitored at 4000 Hz with an electric cell-substrate impedance sensing (ECIS) instrument (Model Zθ, Applied Biophysics).

    Techniques: Permeability, Electric Cell-substrate Impedance Sensing, Staining, Avidin-Biotin Assay

    FIGURE 5 ANXA2 affects endothelial barrier regulation and cell migration. (a) Lysates of control, nonsiRNA and annexin A2-specific siRNA-treated HPAEC cells were analyzed by western blot. (b) Cell viability of control and nonsi- or siRNA-transfected HPAEC was measured by MTT assay 24, 48, and 72 hr after transfection. Cell viability was expressed as percent of viability observed for 0 hr samples. (c) Resistance of nonsi- and siRNA-transfected HPAEC was monitored using ECIS. Cells plated on 8W10E arrays were transfected with nonsiRNA and ANXA2-specific siRNA at 24 hr. Resistance was followed in time. Representative curves show the means ± SD of three independent measurements. (d) In vitro wound healing assays were performed with ECIS to measure the rate of cell migration. Results are presented as means ± SD of four independent measurements for each sample

    Journal: IUBMB life

    Article Title: Dephosphorylation of annexin A2 by protein phosphatase 1 regulates endothelial cell barrier.

    doi: 10.1002/iub.2538

    Figure Lengend Snippet: FIGURE 5 ANXA2 affects endothelial barrier regulation and cell migration. (a) Lysates of control, nonsiRNA and annexin A2-specific siRNA-treated HPAEC cells were analyzed by western blot. (b) Cell viability of control and nonsi- or siRNA-transfected HPAEC was measured by MTT assay 24, 48, and 72 hr after transfection. Cell viability was expressed as percent of viability observed for 0 hr samples. (c) Resistance of nonsi- and siRNA-transfected HPAEC was monitored using ECIS. Cells plated on 8W10E arrays were transfected with nonsiRNA and ANXA2-specific siRNA at 24 hr. Resistance was followed in time. Representative curves show the means ± SD of three independent measurements. (d) In vitro wound healing assays were performed with ECIS to measure the rate of cell migration. Results are presented as means ± SD of four independent measurements for each sample

    Article Snippet: Electric cell-substrate impedance sensing (ECIS) model Zθ (Applied BioPhysics Inc.) was used to monitor endothelial barrier resistance and cell migration using nonsiRNA or ANXA2-specific siRNA-treated cells as described in Reference 46.

    Techniques: Migration, Control, Western Blot, Transfection, MTT Assay, In Vitro

    FIGURE 6 Annexin A2–S100A10 interaction is regulated by PKC. (a) Confluent monolayer of nonsiRNA and ANXA2-specific siRNA-treated HPAEC cells were challenged by PMA (0 hr) and resistance was measured using ECIS. (b) Annexin A2 or S100A10 proteins were immunoprecipitated from control and PMA (1 μM, 30 min)-treated HPAEC cells. Rabbit IgG was used as IP control. IP complexes were analyzed with specific antibodies by western blot

    Journal: IUBMB life

    Article Title: Dephosphorylation of annexin A2 by protein phosphatase 1 regulates endothelial cell barrier.

    doi: 10.1002/iub.2538

    Figure Lengend Snippet: FIGURE 6 Annexin A2–S100A10 interaction is regulated by PKC. (a) Confluent monolayer of nonsiRNA and ANXA2-specific siRNA-treated HPAEC cells were challenged by PMA (0 hr) and resistance was measured using ECIS. (b) Annexin A2 or S100A10 proteins were immunoprecipitated from control and PMA (1 μM, 30 min)-treated HPAEC cells. Rabbit IgG was used as IP control. IP complexes were analyzed with specific antibodies by western blot

    Article Snippet: Electric cell-substrate impedance sensing (ECIS) model Zθ (Applied BioPhysics Inc.) was used to monitor endothelial barrier resistance and cell migration using nonsiRNA or ANXA2-specific siRNA-treated cells as described in Reference 46.

    Techniques: Immunoprecipitation, Control, Western Blot