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ecis ztheta 16w array module  (Applied BioPhysics)


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    Applied BioPhysics ecis ztheta 16w array module
    <t>ECIS</t> measurements of real‐time cell behavior. Quantitation of the delta max‐min of impedance to a dose response of cells to (A) PE ( n = 6, *** P = 0.0008; **** P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA) and (B) adenosine ( n = 6, P = 0.4751; P = 0.7496; * P = 0.0211; **** P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA). Quantitation of the delta max‐min of impedance to a dose response of cells to (C) α‐adrenergic blocker ( n = 6, P = 0.9957, P = 0.9796, **** P ≤ 0.0001, one‐way ANOVA) and (D) adenosine blockade by CGS‐15943 ( n = 6, P = 0.1370, P = 0.9997, **** P ≤ 0.0001, one‐way ANOVA). Data are presented as the mean ± SD.
    Ecis Ztheta 16w Array Module, supplied by Applied BioPhysics, used in various techniques. Bioz Stars score: 96/100, based on 229 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ecis+ztheta+16w+array+module/ECIS+96W+Station/pmc07780101-130-13-18
    Average 96 stars, based on 229 article reviews
    ecis ztheta 16w array module - by Bioz Stars, 2026-09
    96/100 stars

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    1) Product Images from "Cardiac pericytes function as key vasoactive cells to regulate homeostasis and disease"

    Article Title: Cardiac pericytes function as key vasoactive cells to regulate homeostasis and disease

    Journal: FEBS Open Bio

    doi: 10.1002/2211-5463.13021

    ECIS measurements of real‐time cell behavior. Quantitation of the delta max‐min of impedance to a dose response of cells to (A) PE ( n = 6, *** P = 0.0008; **** P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA) and (B) adenosine ( n = 6, P = 0.4751; P = 0.7496; * P = 0.0211; **** P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA). Quantitation of the delta max‐min of impedance to a dose response of cells to (C) α‐adrenergic blocker ( n = 6, P = 0.9957, P = 0.9796, **** P ≤ 0.0001, one‐way ANOVA) and (D) adenosine blockade by CGS‐15943 ( n = 6, P = 0.1370, P = 0.9997, **** P ≤ 0.0001, one‐way ANOVA). Data are presented as the mean ± SD.
    Figure Legend Snippet: ECIS measurements of real‐time cell behavior. Quantitation of the delta max‐min of impedance to a dose response of cells to (A) PE ( n = 6, *** P = 0.0008; **** P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA) and (B) adenosine ( n = 6, P = 0.4751; P = 0.7496; * P = 0.0211; **** P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA). Quantitation of the delta max‐min of impedance to a dose response of cells to (C) α‐adrenergic blocker ( n = 6, P = 0.9957, P = 0.9796, **** P ≤ 0.0001, one‐way ANOVA) and (D) adenosine blockade by CGS‐15943 ( n = 6, P = 0.1370, P = 0.9997, **** P ≤ 0.0001, one‐way ANOVA). Data are presented as the mean ± SD.

    Techniques Used: Quantitation Assay

    Cardiac PCs were subjected to hypoxic conditions (2%) for 24 or 48 h. (A) HIF‐1α translocation after 24 h (B) Quantification of nuclear to total fluorescence of HIF‐1α protein ( n = 4, **** P ≤ 0.0001, Student's unpaired t ‐test). (C) HIF‐1α protein expression increased significantly after 24 h normalized to GAPDH ( n = 6, **** P ≤ 0.0001, Student's unpaired t ‐test). (D) Cell viability was determined over the course of 4 days. Angiogenic factors (E) PDGFbb ( n = 8, * P = 0.0005 Student's unpaired t ‐test) and VEGF‐A ( n = 8, **** P ≤ 0.0001, Student's unpaired t ‐test) were significantly increased after 48 h. (F) Apoptosis was determined by AV5 expression and PI staining where there was a significant difference between normoxic and hypoxic conditions after 48 h ( n = 3, P = 0.7802, **** P ≤ 0.0001, P ≤ 0.0001, one‐way ANOVA). ECIS measurements of real‐time cell behavior. Quantitation of the delta max‐min of impedance to a dose response of cells to (G) chemical ischemia ( n = 6, * P = 0.0144, **** P ≤ 0.0001, P ≤ 0.0001, one‐way ANOVA). Data are presented as the mean ± SD. Scale bar = 100 µm.
    Figure Legend Snippet: Cardiac PCs were subjected to hypoxic conditions (2%) for 24 or 48 h. (A) HIF‐1α translocation after 24 h (B) Quantification of nuclear to total fluorescence of HIF‐1α protein ( n = 4, **** P ≤ 0.0001, Student's unpaired t ‐test). (C) HIF‐1α protein expression increased significantly after 24 h normalized to GAPDH ( n = 6, **** P ≤ 0.0001, Student's unpaired t ‐test). (D) Cell viability was determined over the course of 4 days. Angiogenic factors (E) PDGFbb ( n = 8, * P = 0.0005 Student's unpaired t ‐test) and VEGF‐A ( n = 8, **** P ≤ 0.0001, Student's unpaired t ‐test) were significantly increased after 48 h. (F) Apoptosis was determined by AV5 expression and PI staining where there was a significant difference between normoxic and hypoxic conditions after 48 h ( n = 3, P = 0.7802, **** P ≤ 0.0001, P ≤ 0.0001, one‐way ANOVA). ECIS measurements of real‐time cell behavior. Quantitation of the delta max‐min of impedance to a dose response of cells to (G) chemical ischemia ( n = 6, * P = 0.0144, **** P ≤ 0.0001, P ≤ 0.0001, one‐way ANOVA). Data are presented as the mean ± SD. Scale bar = 100 µm.

    Techniques Used: Translocation Assay, Fluorescence, Expressing, Staining, Quantitation Assay

    Effects of 24 h of LDL treatment on cardiac PCs. (A) Cell proliferation decreased upon high LDL treatment at 250 µg·mL −1 but no changes at 50 µg·mL −1 . (B) Cardiac PCs formed lipid droplets (neutral lipid staining with Oil Red O and counterstained with hematoxcylin) in response to 24 h of LDL treatment. Images taken at 10×. Black arrows point to lipid droplets in the cytoplasm at 40x after treatment at 250 µg·mL −1 . (C) Fold change in mRNA levels normalized to GAPDH. ADFP mRNA levels increased significantly upon increasing concentrations of LDL treatment ( n = 3, ** P = 0.0012, **** P < 0.0001, P < 0.0001, one‐way ANOVA). (D) Protein expression normalized to GAPDH. There is a significant increase in perilipin‐2 protein expression upon LDL treatment at 250 µg·mL −1 but not at 50 µg·mL −1 ( n = 3, P = 0.5173, **** P < 0.0001, P < 0.0001, one‐way ANOVA). ECIS measurements of real‐time cell behavior. (E) Quantitation of the delta max‐min of cell impedance to LDL treatment at 50 or 250 µg·mL −1 with or without PE‐induced contraction ( n = 6, **** P < 0.0001, two‐way ANOVA). Data are presented as the mean ± SD. Scale bar = 200 µm for 10× images. Scale bar = 100 µm for 40× image.
    Figure Legend Snippet: Effects of 24 h of LDL treatment on cardiac PCs. (A) Cell proliferation decreased upon high LDL treatment at 250 µg·mL −1 but no changes at 50 µg·mL −1 . (B) Cardiac PCs formed lipid droplets (neutral lipid staining with Oil Red O and counterstained with hematoxcylin) in response to 24 h of LDL treatment. Images taken at 10×. Black arrows point to lipid droplets in the cytoplasm at 40x after treatment at 250 µg·mL −1 . (C) Fold change in mRNA levels normalized to GAPDH. ADFP mRNA levels increased significantly upon increasing concentrations of LDL treatment ( n = 3, ** P = 0.0012, **** P < 0.0001, P < 0.0001, one‐way ANOVA). (D) Protein expression normalized to GAPDH. There is a significant increase in perilipin‐2 protein expression upon LDL treatment at 250 µg·mL −1 but not at 50 µg·mL −1 ( n = 3, P = 0.5173, **** P < 0.0001, P < 0.0001, one‐way ANOVA). ECIS measurements of real‐time cell behavior. (E) Quantitation of the delta max‐min of cell impedance to LDL treatment at 50 or 250 µg·mL −1 with or without PE‐induced contraction ( n = 6, **** P < 0.0001, two‐way ANOVA). Data are presented as the mean ± SD. Scale bar = 200 µm for 10× images. Scale bar = 100 µm for 40× image.

    Techniques Used: Staining, Expressing, Quantitation Assay

    Effects of 24 h of elevated d ‐glucose levels on cardiac PCs. (A) Cell proliferation was unaffected by increased glucose levels at 50 m m but cells died at low glucose levels of 5.5 m m . (B) Fold change in mRNA levels of common cytokines in diabetic conditions normalized to GAPDH. IL‐6 did not have any changes upon high glucose or high glucose in combination with insulin treatment ( n = 3, P = 0.1016, one‐way ANOVA). CCL2 increased significantly upon high glucose treatment without and with insulin ( n = 3, ** P = 0.01154 and * P = 0.02269, one‐way ANOVA). TNF‐α increased significantly upon high glucose treatment without and with insulin ( n = 3, **** P = 0.00751 and * P = 0.000738, one‐way ANOVA). (C) Protein expression of common cytokines. IL‐6 protein levels decreased significantly upon high glucose treatment with and without insulin ( n = 3, ** P = 0.0064 and * P = 0.0359, one‐way ANOVA). CCL2 protein levels did not significantly increase upon high glucose treatment but it did significantly increase upon high glucose treatment with insulin ( n = 3, P = 0.2457 and * P = 0.0472, one‐way ANOVA). ECIS measurements of real‐time cell behavior. (D) Quantitation of the delta max‐min of cell impedance to high glucose or high glucose plus insulin treatment with or without PE‐induced contraction ( n = 14, P = 0.4841, P = 0.9230, P = 0.0901, two‐way ANOVA). Data are presented as the mean ± SD.
    Figure Legend Snippet: Effects of 24 h of elevated d ‐glucose levels on cardiac PCs. (A) Cell proliferation was unaffected by increased glucose levels at 50 m m but cells died at low glucose levels of 5.5 m m . (B) Fold change in mRNA levels of common cytokines in diabetic conditions normalized to GAPDH. IL‐6 did not have any changes upon high glucose or high glucose in combination with insulin treatment ( n = 3, P = 0.1016, one‐way ANOVA). CCL2 increased significantly upon high glucose treatment without and with insulin ( n = 3, ** P = 0.01154 and * P = 0.02269, one‐way ANOVA). TNF‐α increased significantly upon high glucose treatment without and with insulin ( n = 3, **** P = 0.00751 and * P = 0.000738, one‐way ANOVA). (C) Protein expression of common cytokines. IL‐6 protein levels decreased significantly upon high glucose treatment with and without insulin ( n = 3, ** P = 0.0064 and * P = 0.0359, one‐way ANOVA). CCL2 protein levels did not significantly increase upon high glucose treatment but it did significantly increase upon high glucose treatment with insulin ( n = 3, P = 0.2457 and * P = 0.0472, one‐way ANOVA). ECIS measurements of real‐time cell behavior. (D) Quantitation of the delta max‐min of cell impedance to high glucose or high glucose plus insulin treatment with or without PE‐induced contraction ( n = 14, P = 0.4841, P = 0.9230, P = 0.0901, two‐way ANOVA). Data are presented as the mean ± SD.

    Techniques Used: Expressing, Quantitation Assay

    Related Articles

    Electric Cell-substrate Impedance Sensing:

    Article Title: Cardiac pericytes function as key vasoactive cells to regulate homeostasis and disease
    Article Snippet: PCs were grown on the bottom of the Transwell filter adaptor (Applied Biophysics Inc.) coated with gelatin (Applied Biophysics Inc.) at 500 000 cells/mL in 1 mL of DMEM + 5% FBS + 1% P/S. .. Inserts were placed into a Transwell filter adapter and then moved to the ECIS Ztheta 16W array module (Applied Biophysics Inc., Troy, NY, USA) inside a cell incubator at 37 °C and 5% CO 2 . ..



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    Applied BioPhysics ecis ztheta 16w array module
    <t>ECIS</t> measurements of real‐time cell behavior. Quantitation of the delta max‐min of impedance to a dose response of cells to (A) PE ( n = 6, *** P = 0.0008; **** P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA) and (B) adenosine ( n = 6, P = 0.4751; P = 0.7496; * P = 0.0211; **** P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA). Quantitation of the delta max‐min of impedance to a dose response of cells to (C) α‐adrenergic blocker ( n = 6, P = 0.9957, P = 0.9796, **** P ≤ 0.0001, one‐way ANOVA) and (D) adenosine blockade by CGS‐15943 ( n = 6, P = 0.1370, P = 0.9997, **** P ≤ 0.0001, one‐way ANOVA). Data are presented as the mean ± SD.
    Ecis Ztheta 16w Array Module, supplied by Applied BioPhysics, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ecis+ztheta+16w+array+module/ECIS+96W+Station/pmc07780101-130-13-18
    Average 96 stars, based on 1 article reviews
    ecis ztheta 16w array module - by Bioz Stars, 2026-09
    96/100 stars
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    ECIS measurements of real‐time cell behavior. Quantitation of the delta max‐min of impedance to a dose response of cells to (A) PE ( n = 6, *** P = 0.0008; **** P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA) and (B) adenosine ( n = 6, P = 0.4751; P = 0.7496; * P = 0.0211; **** P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA). Quantitation of the delta max‐min of impedance to a dose response of cells to (C) α‐adrenergic blocker ( n = 6, P = 0.9957, P = 0.9796, **** P ≤ 0.0001, one‐way ANOVA) and (D) adenosine blockade by CGS‐15943 ( n = 6, P = 0.1370, P = 0.9997, **** P ≤ 0.0001, one‐way ANOVA). Data are presented as the mean ± SD.

    Journal: FEBS Open Bio

    Article Title: Cardiac pericytes function as key vasoactive cells to regulate homeostasis and disease

    doi: 10.1002/2211-5463.13021

    Figure Lengend Snippet: ECIS measurements of real‐time cell behavior. Quantitation of the delta max‐min of impedance to a dose response of cells to (A) PE ( n = 6, *** P = 0.0008; **** P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA) and (B) adenosine ( n = 6, P = 0.4751; P = 0.7496; * P = 0.0211; **** P ≤ 0.0001; P ≤ 0.0001, one‐way ANOVA). Quantitation of the delta max‐min of impedance to a dose response of cells to (C) α‐adrenergic blocker ( n = 6, P = 0.9957, P = 0.9796, **** P ≤ 0.0001, one‐way ANOVA) and (D) adenosine blockade by CGS‐15943 ( n = 6, P = 0.1370, P = 0.9997, **** P ≤ 0.0001, one‐way ANOVA). Data are presented as the mean ± SD.

    Article Snippet: Inserts were placed into a Transwell filter adapter and then moved to the ECIS Ztheta 16W array module (Applied Biophysics Inc., Troy, NY, USA) inside a cell incubator at 37 °C and 5% CO 2 .

    Techniques: Quantitation Assay

    Cardiac PCs were subjected to hypoxic conditions (2%) for 24 or 48 h. (A) HIF‐1α translocation after 24 h (B) Quantification of nuclear to total fluorescence of HIF‐1α protein ( n = 4, **** P ≤ 0.0001, Student's unpaired t ‐test). (C) HIF‐1α protein expression increased significantly after 24 h normalized to GAPDH ( n = 6, **** P ≤ 0.0001, Student's unpaired t ‐test). (D) Cell viability was determined over the course of 4 days. Angiogenic factors (E) PDGFbb ( n = 8, * P = 0.0005 Student's unpaired t ‐test) and VEGF‐A ( n = 8, **** P ≤ 0.0001, Student's unpaired t ‐test) were significantly increased after 48 h. (F) Apoptosis was determined by AV5 expression and PI staining where there was a significant difference between normoxic and hypoxic conditions after 48 h ( n = 3, P = 0.7802, **** P ≤ 0.0001, P ≤ 0.0001, one‐way ANOVA). ECIS measurements of real‐time cell behavior. Quantitation of the delta max‐min of impedance to a dose response of cells to (G) chemical ischemia ( n = 6, * P = 0.0144, **** P ≤ 0.0001, P ≤ 0.0001, one‐way ANOVA). Data are presented as the mean ± SD. Scale bar = 100 µm.

    Journal: FEBS Open Bio

    Article Title: Cardiac pericytes function as key vasoactive cells to regulate homeostasis and disease

    doi: 10.1002/2211-5463.13021

    Figure Lengend Snippet: Cardiac PCs were subjected to hypoxic conditions (2%) for 24 or 48 h. (A) HIF‐1α translocation after 24 h (B) Quantification of nuclear to total fluorescence of HIF‐1α protein ( n = 4, **** P ≤ 0.0001, Student's unpaired t ‐test). (C) HIF‐1α protein expression increased significantly after 24 h normalized to GAPDH ( n = 6, **** P ≤ 0.0001, Student's unpaired t ‐test). (D) Cell viability was determined over the course of 4 days. Angiogenic factors (E) PDGFbb ( n = 8, * P = 0.0005 Student's unpaired t ‐test) and VEGF‐A ( n = 8, **** P ≤ 0.0001, Student's unpaired t ‐test) were significantly increased after 48 h. (F) Apoptosis was determined by AV5 expression and PI staining where there was a significant difference between normoxic and hypoxic conditions after 48 h ( n = 3, P = 0.7802, **** P ≤ 0.0001, P ≤ 0.0001, one‐way ANOVA). ECIS measurements of real‐time cell behavior. Quantitation of the delta max‐min of impedance to a dose response of cells to (G) chemical ischemia ( n = 6, * P = 0.0144, **** P ≤ 0.0001, P ≤ 0.0001, one‐way ANOVA). Data are presented as the mean ± SD. Scale bar = 100 µm.

    Article Snippet: Inserts were placed into a Transwell filter adapter and then moved to the ECIS Ztheta 16W array module (Applied Biophysics Inc., Troy, NY, USA) inside a cell incubator at 37 °C and 5% CO 2 .

    Techniques: Translocation Assay, Fluorescence, Expressing, Staining, Quantitation Assay

    Effects of 24 h of LDL treatment on cardiac PCs. (A) Cell proliferation decreased upon high LDL treatment at 250 µg·mL −1 but no changes at 50 µg·mL −1 . (B) Cardiac PCs formed lipid droplets (neutral lipid staining with Oil Red O and counterstained with hematoxcylin) in response to 24 h of LDL treatment. Images taken at 10×. Black arrows point to lipid droplets in the cytoplasm at 40x after treatment at 250 µg·mL −1 . (C) Fold change in mRNA levels normalized to GAPDH. ADFP mRNA levels increased significantly upon increasing concentrations of LDL treatment ( n = 3, ** P = 0.0012, **** P < 0.0001, P < 0.0001, one‐way ANOVA). (D) Protein expression normalized to GAPDH. There is a significant increase in perilipin‐2 protein expression upon LDL treatment at 250 µg·mL −1 but not at 50 µg·mL −1 ( n = 3, P = 0.5173, **** P < 0.0001, P < 0.0001, one‐way ANOVA). ECIS measurements of real‐time cell behavior. (E) Quantitation of the delta max‐min of cell impedance to LDL treatment at 50 or 250 µg·mL −1 with or without PE‐induced contraction ( n = 6, **** P < 0.0001, two‐way ANOVA). Data are presented as the mean ± SD. Scale bar = 200 µm for 10× images. Scale bar = 100 µm for 40× image.

    Journal: FEBS Open Bio

    Article Title: Cardiac pericytes function as key vasoactive cells to regulate homeostasis and disease

    doi: 10.1002/2211-5463.13021

    Figure Lengend Snippet: Effects of 24 h of LDL treatment on cardiac PCs. (A) Cell proliferation decreased upon high LDL treatment at 250 µg·mL −1 but no changes at 50 µg·mL −1 . (B) Cardiac PCs formed lipid droplets (neutral lipid staining with Oil Red O and counterstained with hematoxcylin) in response to 24 h of LDL treatment. Images taken at 10×. Black arrows point to lipid droplets in the cytoplasm at 40x after treatment at 250 µg·mL −1 . (C) Fold change in mRNA levels normalized to GAPDH. ADFP mRNA levels increased significantly upon increasing concentrations of LDL treatment ( n = 3, ** P = 0.0012, **** P < 0.0001, P < 0.0001, one‐way ANOVA). (D) Protein expression normalized to GAPDH. There is a significant increase in perilipin‐2 protein expression upon LDL treatment at 250 µg·mL −1 but not at 50 µg·mL −1 ( n = 3, P = 0.5173, **** P < 0.0001, P < 0.0001, one‐way ANOVA). ECIS measurements of real‐time cell behavior. (E) Quantitation of the delta max‐min of cell impedance to LDL treatment at 50 or 250 µg·mL −1 with or without PE‐induced contraction ( n = 6, **** P < 0.0001, two‐way ANOVA). Data are presented as the mean ± SD. Scale bar = 200 µm for 10× images. Scale bar = 100 µm for 40× image.

    Article Snippet: Inserts were placed into a Transwell filter adapter and then moved to the ECIS Ztheta 16W array module (Applied Biophysics Inc., Troy, NY, USA) inside a cell incubator at 37 °C and 5% CO 2 .

    Techniques: Staining, Expressing, Quantitation Assay

    Effects of 24 h of elevated d ‐glucose levels on cardiac PCs. (A) Cell proliferation was unaffected by increased glucose levels at 50 m m but cells died at low glucose levels of 5.5 m m . (B) Fold change in mRNA levels of common cytokines in diabetic conditions normalized to GAPDH. IL‐6 did not have any changes upon high glucose or high glucose in combination with insulin treatment ( n = 3, P = 0.1016, one‐way ANOVA). CCL2 increased significantly upon high glucose treatment without and with insulin ( n = 3, ** P = 0.01154 and * P = 0.02269, one‐way ANOVA). TNF‐α increased significantly upon high glucose treatment without and with insulin ( n = 3, **** P = 0.00751 and * P = 0.000738, one‐way ANOVA). (C) Protein expression of common cytokines. IL‐6 protein levels decreased significantly upon high glucose treatment with and without insulin ( n = 3, ** P = 0.0064 and * P = 0.0359, one‐way ANOVA). CCL2 protein levels did not significantly increase upon high glucose treatment but it did significantly increase upon high glucose treatment with insulin ( n = 3, P = 0.2457 and * P = 0.0472, one‐way ANOVA). ECIS measurements of real‐time cell behavior. (D) Quantitation of the delta max‐min of cell impedance to high glucose or high glucose plus insulin treatment with or without PE‐induced contraction ( n = 14, P = 0.4841, P = 0.9230, P = 0.0901, two‐way ANOVA). Data are presented as the mean ± SD.

    Journal: FEBS Open Bio

    Article Title: Cardiac pericytes function as key vasoactive cells to regulate homeostasis and disease

    doi: 10.1002/2211-5463.13021

    Figure Lengend Snippet: Effects of 24 h of elevated d ‐glucose levels on cardiac PCs. (A) Cell proliferation was unaffected by increased glucose levels at 50 m m but cells died at low glucose levels of 5.5 m m . (B) Fold change in mRNA levels of common cytokines in diabetic conditions normalized to GAPDH. IL‐6 did not have any changes upon high glucose or high glucose in combination with insulin treatment ( n = 3, P = 0.1016, one‐way ANOVA). CCL2 increased significantly upon high glucose treatment without and with insulin ( n = 3, ** P = 0.01154 and * P = 0.02269, one‐way ANOVA). TNF‐α increased significantly upon high glucose treatment without and with insulin ( n = 3, **** P = 0.00751 and * P = 0.000738, one‐way ANOVA). (C) Protein expression of common cytokines. IL‐6 protein levels decreased significantly upon high glucose treatment with and without insulin ( n = 3, ** P = 0.0064 and * P = 0.0359, one‐way ANOVA). CCL2 protein levels did not significantly increase upon high glucose treatment but it did significantly increase upon high glucose treatment with insulin ( n = 3, P = 0.2457 and * P = 0.0472, one‐way ANOVA). ECIS measurements of real‐time cell behavior. (D) Quantitation of the delta max‐min of cell impedance to high glucose or high glucose plus insulin treatment with or without PE‐induced contraction ( n = 14, P = 0.4841, P = 0.9230, P = 0.0901, two‐way ANOVA). Data are presented as the mean ± SD.

    Article Snippet: Inserts were placed into a Transwell filter adapter and then moved to the ECIS Ztheta 16W array module (Applied Biophysics Inc., Troy, NY, USA) inside a cell incubator at 37 °C and 5% CO 2 .

    Techniques: Expressing, Quantitation Assay