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igfbp 3 levels  (R&D Systems)


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    R&D Systems igfbp 3 levels
    <t>IGFBP-3</t> blocks the hyperosmolarity-induced decrease in mitochondrial respiration and glycolysis in corneal epithelial cells. The hTCEpi cells were cultured in basal media with or without hyperosmolar conditions for 24 hours. Cells cultured in 450 mOsM were cotreated with 500 ng/mL rhIGFBP-3. ( A ) IGFBP-3 secretion was down regulated in hyperosmolar culture in basal media ( * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) Immunoblotting for intracellular IGFBP-3 in whole cell lysates. Consistent with the decrease in secreted IGFBP-3, intracellular IGFBP-3 was also sequentially decreased with increasing levels of salt. Beta-actin was used as a loading control. ( C ) Consistent with our prior results, both respiration and glycolysis were significantly decreased after culture in 450 mOsM/kg ( ** P = 0.021 and *** P = 0.011, one-way ANOVA, SNK multiple comparison test, n = 3). Treatment with rhIGFBP-3 restored metabolism and glycolysis to basal levels ( **** P = 0.042 and ***** P = 0.012, one-way ANOVA, SNK multiple comparison test, n = 3). ( D ) Hyperosmolar culture shifted cells toward a respiratory phenotype in hyperosmolar culture that was restored following treatment with rhIGFBP-3 ( ****** P = 0.002 and * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( E ) SYBR green staining for mitochondrial DNA showed a decrease in mtDNA after hyperosmolar culture that was blocked by co-treatment with rhIGFBP-3. Scale bar : 10 µm. Number indicates mOsM. Images representative of three repeated experiments.
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    Images

    1) Product Images from "IGFBP-3 Mediates Metabolic Homeostasis During Hyperosmolar Stress in the Corneal Epithelium"

    Article Title: IGFBP-3 Mediates Metabolic Homeostasis During Hyperosmolar Stress in the Corneal Epithelium

    Journal: Investigative Ophthalmology & Visual Science

    doi: 10.1167/iovs.62.7.11

    IGFBP-3 blocks the hyperosmolarity-induced decrease in mitochondrial respiration and glycolysis in corneal epithelial cells. The hTCEpi cells were cultured in basal media with or without hyperosmolar conditions for 24 hours. Cells cultured in 450 mOsM were cotreated with 500 ng/mL rhIGFBP-3. ( A ) IGFBP-3 secretion was down regulated in hyperosmolar culture in basal media ( * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) Immunoblotting for intracellular IGFBP-3 in whole cell lysates. Consistent with the decrease in secreted IGFBP-3, intracellular IGFBP-3 was also sequentially decreased with increasing levels of salt. Beta-actin was used as a loading control. ( C ) Consistent with our prior results, both respiration and glycolysis were significantly decreased after culture in 450 mOsM/kg ( ** P = 0.021 and *** P = 0.011, one-way ANOVA, SNK multiple comparison test, n = 3). Treatment with rhIGFBP-3 restored metabolism and glycolysis to basal levels ( **** P = 0.042 and ***** P = 0.012, one-way ANOVA, SNK multiple comparison test, n = 3). ( D ) Hyperosmolar culture shifted cells toward a respiratory phenotype in hyperosmolar culture that was restored following treatment with rhIGFBP-3 ( ****** P = 0.002 and * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( E ) SYBR green staining for mitochondrial DNA showed a decrease in mtDNA after hyperosmolar culture that was blocked by co-treatment with rhIGFBP-3. Scale bar : 10 µm. Number indicates mOsM. Images representative of three repeated experiments.
    Figure Legend Snippet: IGFBP-3 blocks the hyperosmolarity-induced decrease in mitochondrial respiration and glycolysis in corneal epithelial cells. The hTCEpi cells were cultured in basal media with or without hyperosmolar conditions for 24 hours. Cells cultured in 450 mOsM were cotreated with 500 ng/mL rhIGFBP-3. ( A ) IGFBP-3 secretion was down regulated in hyperosmolar culture in basal media ( * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) Immunoblotting for intracellular IGFBP-3 in whole cell lysates. Consistent with the decrease in secreted IGFBP-3, intracellular IGFBP-3 was also sequentially decreased with increasing levels of salt. Beta-actin was used as a loading control. ( C ) Consistent with our prior results, both respiration and glycolysis were significantly decreased after culture in 450 mOsM/kg ( ** P = 0.021 and *** P = 0.011, one-way ANOVA, SNK multiple comparison test, n = 3). Treatment with rhIGFBP-3 restored metabolism and glycolysis to basal levels ( **** P = 0.042 and ***** P = 0.012, one-way ANOVA, SNK multiple comparison test, n = 3). ( D ) Hyperosmolar culture shifted cells toward a respiratory phenotype in hyperosmolar culture that was restored following treatment with rhIGFBP-3 ( ****** P = 0.002 and * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( E ) SYBR green staining for mitochondrial DNA showed a decrease in mtDNA after hyperosmolar culture that was blocked by co-treatment with rhIGFBP-3. Scale bar : 10 µm. Number indicates mOsM. Images representative of three repeated experiments.

    Techniques Used: Cell Culture, Comparison, Western Blot, SYBR Green Assay, Staining

    Hyperosmolar culture induced expression of the anti-inflammatory cytokines, IL-6 and IL-8. hTCEpi cells were cultured in basal media in isotonic and hyperosmolar conditions with and without 500 ng/mL rhIGFBP-3 for 24 hours. ( A ) Hyperosmolar culture triggered release of IL-6 that was not affected by treatment with rhIGFBP-3 ( * P = 0.008 for 450 compared to KBM, ** P = 0.004 for IGFBP-3 treated cells in hyperosmolar culture compared to KBM, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) IL-8 showed a more robust increase in hyperosmolar culture compared to KBM ( * P = 0.001). This increase was partially abrogated by treatment with rhIGFBP-3 ( ** P = 0.033, one-way ANOVA, SNK multiple comparison test). Data represented as mean ± standard deviation.
    Figure Legend Snippet: Hyperosmolar culture induced expression of the anti-inflammatory cytokines, IL-6 and IL-8. hTCEpi cells were cultured in basal media in isotonic and hyperosmolar conditions with and without 500 ng/mL rhIGFBP-3 for 24 hours. ( A ) Hyperosmolar culture triggered release of IL-6 that was not affected by treatment with rhIGFBP-3 ( * P = 0.008 for 450 compared to KBM, ** P = 0.004 for IGFBP-3 treated cells in hyperosmolar culture compared to KBM, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) IL-8 showed a more robust increase in hyperosmolar culture compared to KBM ( * P = 0.001). This increase was partially abrogated by treatment with rhIGFBP-3 ( ** P = 0.033, one-way ANOVA, SNK multiple comparison test). Data represented as mean ± standard deviation.

    Techniques Used: Expressing, Cell Culture, Comparison, Standard Deviation



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    <t>IGFBP-3</t> blocks the hyperosmolarity-induced decrease in mitochondrial respiration and glycolysis in corneal epithelial cells. The hTCEpi cells were cultured in basal media with or without hyperosmolar conditions for 24 hours. Cells cultured in 450 mOsM were cotreated with 500 ng/mL rhIGFBP-3. ( A ) IGFBP-3 secretion was down regulated in hyperosmolar culture in basal media ( * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) Immunoblotting for intracellular IGFBP-3 in whole cell lysates. Consistent with the decrease in secreted IGFBP-3, intracellular IGFBP-3 was also sequentially decreased with increasing levels of salt. Beta-actin was used as a loading control. ( C ) Consistent with our prior results, both respiration and glycolysis were significantly decreased after culture in 450 mOsM/kg ( ** P = 0.021 and *** P = 0.011, one-way ANOVA, SNK multiple comparison test, n = 3). Treatment with rhIGFBP-3 restored metabolism and glycolysis to basal levels ( **** P = 0.042 and ***** P = 0.012, one-way ANOVA, SNK multiple comparison test, n = 3). ( D ) Hyperosmolar culture shifted cells toward a respiratory phenotype in hyperosmolar culture that was restored following treatment with rhIGFBP-3 ( ****** P = 0.002 and * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( E ) SYBR green staining for mitochondrial DNA showed a decrease in mtDNA after hyperosmolar culture that was blocked by co-treatment with rhIGFBP-3. Scale bar : 10 µm. Number indicates mOsM. Images representative of three repeated experiments.
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    <t>IGFBP-3</t> blocks the hyperosmolarity-induced decrease in mitochondrial respiration and glycolysis in corneal epithelial cells. The hTCEpi cells were cultured in basal media with or without hyperosmolar conditions for 24 hours. Cells cultured in 450 mOsM were cotreated with 500 ng/mL rhIGFBP-3. ( A ) IGFBP-3 secretion was down regulated in hyperosmolar culture in basal media ( * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) Immunoblotting for intracellular IGFBP-3 in whole cell lysates. Consistent with the decrease in secreted IGFBP-3, intracellular IGFBP-3 was also sequentially decreased with increasing levels of salt. Beta-actin was used as a loading control. ( C ) Consistent with our prior results, both respiration and glycolysis were significantly decreased after culture in 450 mOsM/kg ( ** P = 0.021 and *** P = 0.011, one-way ANOVA, SNK multiple comparison test, n = 3). Treatment with rhIGFBP-3 restored metabolism and glycolysis to basal levels ( **** P = 0.042 and ***** P = 0.012, one-way ANOVA, SNK multiple comparison test, n = 3). ( D ) Hyperosmolar culture shifted cells toward a respiratory phenotype in hyperosmolar culture that was restored following treatment with rhIGFBP-3 ( ****** P = 0.002 and * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( E ) SYBR green staining for mitochondrial DNA showed a decrease in mtDNA after hyperosmolar culture that was blocked by co-treatment with rhIGFBP-3. Scale bar : 10 µm. Number indicates mOsM. Images representative of three repeated experiments.
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    Image Search Results


    IGFBP-3 blocks the hyperosmolarity-induced decrease in mitochondrial respiration and glycolysis in corneal epithelial cells. The hTCEpi cells were cultured in basal media with or without hyperosmolar conditions for 24 hours. Cells cultured in 450 mOsM were cotreated with 500 ng/mL rhIGFBP-3. ( A ) IGFBP-3 secretion was down regulated in hyperosmolar culture in basal media ( * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) Immunoblotting for intracellular IGFBP-3 in whole cell lysates. Consistent with the decrease in secreted IGFBP-3, intracellular IGFBP-3 was also sequentially decreased with increasing levels of salt. Beta-actin was used as a loading control. ( C ) Consistent with our prior results, both respiration and glycolysis were significantly decreased after culture in 450 mOsM/kg ( ** P = 0.021 and *** P = 0.011, one-way ANOVA, SNK multiple comparison test, n = 3). Treatment with rhIGFBP-3 restored metabolism and glycolysis to basal levels ( **** P = 0.042 and ***** P = 0.012, one-way ANOVA, SNK multiple comparison test, n = 3). ( D ) Hyperosmolar culture shifted cells toward a respiratory phenotype in hyperosmolar culture that was restored following treatment with rhIGFBP-3 ( ****** P = 0.002 and * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( E ) SYBR green staining for mitochondrial DNA showed a decrease in mtDNA after hyperosmolar culture that was blocked by co-treatment with rhIGFBP-3. Scale bar : 10 µm. Number indicates mOsM. Images representative of three repeated experiments.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: IGFBP-3 Mediates Metabolic Homeostasis During Hyperosmolar Stress in the Corneal Epithelium

    doi: 10.1167/iovs.62.7.11

    Figure Lengend Snippet: IGFBP-3 blocks the hyperosmolarity-induced decrease in mitochondrial respiration and glycolysis in corneal epithelial cells. The hTCEpi cells were cultured in basal media with or without hyperosmolar conditions for 24 hours. Cells cultured in 450 mOsM were cotreated with 500 ng/mL rhIGFBP-3. ( A ) IGFBP-3 secretion was down regulated in hyperosmolar culture in basal media ( * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) Immunoblotting for intracellular IGFBP-3 in whole cell lysates. Consistent with the decrease in secreted IGFBP-3, intracellular IGFBP-3 was also sequentially decreased with increasing levels of salt. Beta-actin was used as a loading control. ( C ) Consistent with our prior results, both respiration and glycolysis were significantly decreased after culture in 450 mOsM/kg ( ** P = 0.021 and *** P = 0.011, one-way ANOVA, SNK multiple comparison test, n = 3). Treatment with rhIGFBP-3 restored metabolism and glycolysis to basal levels ( **** P = 0.042 and ***** P = 0.012, one-way ANOVA, SNK multiple comparison test, n = 3). ( D ) Hyperosmolar culture shifted cells toward a respiratory phenotype in hyperosmolar culture that was restored following treatment with rhIGFBP-3 ( ****** P = 0.002 and * P < 0.001, one-way ANOVA, SNK multiple comparison test, n = 3). ( E ) SYBR green staining for mitochondrial DNA showed a decrease in mtDNA after hyperosmolar culture that was blocked by co-treatment with rhIGFBP-3. Scale bar : 10 µm. Number indicates mOsM. Images representative of three repeated experiments.

    Article Snippet: A solid phase sandwich ELISA was used to quantify IGFBP-3 levels (human Quantikine ELISA; R&D Systems, Minneapolis, MN, USA).

    Techniques: Cell Culture, Comparison, Western Blot, SYBR Green Assay, Staining

    Hyperosmolar culture induced expression of the anti-inflammatory cytokines, IL-6 and IL-8. hTCEpi cells were cultured in basal media in isotonic and hyperosmolar conditions with and without 500 ng/mL rhIGFBP-3 for 24 hours. ( A ) Hyperosmolar culture triggered release of IL-6 that was not affected by treatment with rhIGFBP-3 ( * P = 0.008 for 450 compared to KBM, ** P = 0.004 for IGFBP-3 treated cells in hyperosmolar culture compared to KBM, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) IL-8 showed a more robust increase in hyperosmolar culture compared to KBM ( * P = 0.001). This increase was partially abrogated by treatment with rhIGFBP-3 ( ** P = 0.033, one-way ANOVA, SNK multiple comparison test). Data represented as mean ± standard deviation.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: IGFBP-3 Mediates Metabolic Homeostasis During Hyperosmolar Stress in the Corneal Epithelium

    doi: 10.1167/iovs.62.7.11

    Figure Lengend Snippet: Hyperosmolar culture induced expression of the anti-inflammatory cytokines, IL-6 and IL-8. hTCEpi cells were cultured in basal media in isotonic and hyperosmolar conditions with and without 500 ng/mL rhIGFBP-3 for 24 hours. ( A ) Hyperosmolar culture triggered release of IL-6 that was not affected by treatment with rhIGFBP-3 ( * P = 0.008 for 450 compared to KBM, ** P = 0.004 for IGFBP-3 treated cells in hyperosmolar culture compared to KBM, one-way ANOVA, SNK multiple comparison test, n = 3). ( B ) IL-8 showed a more robust increase in hyperosmolar culture compared to KBM ( * P = 0.001). This increase was partially abrogated by treatment with rhIGFBP-3 ( ** P = 0.033, one-way ANOVA, SNK multiple comparison test). Data represented as mean ± standard deviation.

    Article Snippet: A solid phase sandwich ELISA was used to quantify IGFBP-3 levels (human Quantikine ELISA; R&D Systems, Minneapolis, MN, USA).

    Techniques: Expressing, Cell Culture, Comparison, Standard Deviation