vegf  (Millipore)


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    • 99
    Name:
    LH Rabbit Polyclonal Antibody
    Description:
    Anti LH is a useful marker in classification of pituitary tumors and the study of pituitary disease It reacts with LH producing cells gonadotrophs
    Catalog Number:
    209a-1
    Price:
    None
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    Structured Review

    Millipore vegf
    LH Rabbit Polyclonal Antibody
    Anti LH is a useful marker in classification of pituitary tumors and the study of pituitary disease It reacts with LH producing cells gonadotrophs
    https://www.bioz.com/result/vegf/product/Millipore
    Average 99 stars, based on 96 article reviews
    Price from $9.99 to $1999.99
    vegf - by Bioz Stars, 2021-01
    99/100 stars

    Related Products / Commonly Used Together

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    igf-1
    matrigel
    p53
    elisa kits

    Images

    1) Product Images from "Tanshinone IIA potentiates the efficacy of 5-FU in Colo205 colon cancer cells in vivo through downregulation of P-gp and LC3-II"

    Article Title: Tanshinone IIA potentiates the efficacy of 5-FU in Colo205 colon cancer cells in vivo through downregulation of P-gp and LC3-II

    Journal: Experimental and Therapeutic Medicine

    doi: 10.3892/etm.2011.441

    Our results showed that co-treatment with Tan-IIA plus 5-FU in the Colo205 xenograft model decreased the protein expressions of (A) P-gp, (B) LC3-II, (C) VEGF, (D) NF-κB p65 and (E) MMP-7 when compared to 5-FU only. Values are expressed as the
    Figure Legend Snippet: Our results showed that co-treatment with Tan-IIA plus 5-FU in the Colo205 xenograft model decreased the protein expressions of (A) P-gp, (B) LC3-II, (C) VEGF, (D) NF-κB p65 and (E) MMP-7 when compared to 5-FU only. Values are expressed as the

    Techniques Used:

    2) Product Images from "Expression of astrocyte elevated gene-1 closely correlates with the angiogenesis of gastric cancer"

    Article Title: Expression of astrocyte elevated gene-1 closely correlates with the angiogenesis of gastric cancer

    Journal: Oncology Letters

    doi: 10.3892/ol.2014.1950

    Effects of AEG-1 siRNA on VEGF and HIF-1α expression. MGC-803 cells were transfected with AEG-1 siRNA and Con-siRNA. (A) VEGF and HIF-1α were determined by western blotting. Upper panel shows a representative blot for VEGF and HIF-1α protein, and the lower panel shows the quantification of VEGF and HIF-1α protein levels. (B) VEGF and HIF-1α mRNA were determined by real-time reverse transcription polymerase chain reaction in MGC-803 cells and the levels of VEGF and HIF-1α mRNA are presented as the (VEGF and thrombospondin-1)/GAPDH mRNA ratio. Data are presented as means ± standard deviation of three independent experiments. * P
    Figure Legend Snippet: Effects of AEG-1 siRNA on VEGF and HIF-1α expression. MGC-803 cells were transfected with AEG-1 siRNA and Con-siRNA. (A) VEGF and HIF-1α were determined by western blotting. Upper panel shows a representative blot for VEGF and HIF-1α protein, and the lower panel shows the quantification of VEGF and HIF-1α protein levels. (B) VEGF and HIF-1α mRNA were determined by real-time reverse transcription polymerase chain reaction in MGC-803 cells and the levels of VEGF and HIF-1α mRNA are presented as the (VEGF and thrombospondin-1)/GAPDH mRNA ratio. Data are presented as means ± standard deviation of three independent experiments. * P

    Techniques Used: Expressing, Transfection, Western Blot, Reverse Transcription Polymerase Chain Reaction, Standard Deviation

    3) Product Images from "Exosomes from adipose-derived stem cells overexpressing Nrf2 accelerate cutaneous wound healing by promoting vascularization in a diabetic foot ulcer rat model"

    Article Title: Exosomes from adipose-derived stem cells overexpressing Nrf2 accelerate cutaneous wound healing by promoting vascularization in a diabetic foot ulcer rat model

    Journal: Experimental & Molecular Medicine

    doi: 10.1038/s12276-018-0058-5

    Exosomes (Exos) derived from adipose-derived stem cells (ADSCs) overexpressing Nrf2 prevent high glucose (HG)-induced senescence by inhibiting ROS and inflammatory cytokine expression. a , b The level of Nrf2 in exosomes secreted from ADSCs with or without Nrf2 overexpression. c Proliferation of EPC cells was analyzed by the MTT assay with different concentrations of Exos from ADSCs (ADSC-Exo) or Nrf2 overexpression ADSCs (Nrf2-ADSC-Exo) after exposure to high glucose (HG, 30 mM) for 48 h. d Tube formation capability detected in endothelial progenitor cells (EPCs) stimulated with 50 μg/ml ADSC-Exo or Nrf2-ADSC-Exo for 12 h under HG (30 mM) condition. e – j Western blot analysis and protein expression levels of SMP30, VEGF, VEGFR, and NOX1/4 after stimulation with ADSC-Exo or Nrf2-ADSC-Exo for 12 h under HG (30 mM) condition. GAPDH served as an internal control. The relative protein levels were analyzed, and data are presented as the mean ± SD ( n = 3). *** P
    Figure Legend Snippet: Exosomes (Exos) derived from adipose-derived stem cells (ADSCs) overexpressing Nrf2 prevent high glucose (HG)-induced senescence by inhibiting ROS and inflammatory cytokine expression. a , b The level of Nrf2 in exosomes secreted from ADSCs with or without Nrf2 overexpression. c Proliferation of EPC cells was analyzed by the MTT assay with different concentrations of Exos from ADSCs (ADSC-Exo) or Nrf2 overexpression ADSCs (Nrf2-ADSC-Exo) after exposure to high glucose (HG, 30 mM) for 48 h. d Tube formation capability detected in endothelial progenitor cells (EPCs) stimulated with 50 μg/ml ADSC-Exo or Nrf2-ADSC-Exo for 12 h under HG (30 mM) condition. e – j Western blot analysis and protein expression levels of SMP30, VEGF, VEGFR, and NOX1/4 after stimulation with ADSC-Exo or Nrf2-ADSC-Exo for 12 h under HG (30 mM) condition. GAPDH served as an internal control. The relative protein levels were analyzed, and data are presented as the mean ± SD ( n = 3). *** P

    Techniques Used: Derivative Assay, Expressing, Over Expression, MTT Assay, Western Blot

    4) Product Images from "Deletion of Thioredoxin Interacting Protein (TXNIP) Augments Hyperoxia-Induced Vaso-Obliteration in a Mouse Model of Oxygen Induced-Retinopathy"

    Article Title: Deletion of Thioredoxin Interacting Protein (TXNIP) Augments Hyperoxia-Induced Vaso-Obliteration in a Mouse Model of Oxygen Induced-Retinopathy

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0110388

    Deletion of TXNIP does not alter VEGFR2/Akt activation under hyperoxia. Wild type (WT) and TXNIP knockout (TKO) mice were subjected to hyperoxia (75% O2, p7–p12). Activation of VEGFR2 ( A ) and Akt ( B ) were examined as downstream signal of VEGF in p12 WT and TKO retinas. TKO showed significant decrease in phosphorylation of VEGFR-2 and Akt compared to WT under normoxic condition. We did not detect significant change in the activation of VEGFR2 and its downstream Akt in retinas from TKO and WT in response to hyperoxia. (*P
    Figure Legend Snippet: Deletion of TXNIP does not alter VEGFR2/Akt activation under hyperoxia. Wild type (WT) and TXNIP knockout (TKO) mice were subjected to hyperoxia (75% O2, p7–p12). Activation of VEGFR2 ( A ) and Akt ( B ) were examined as downstream signal of VEGF in p12 WT and TKO retinas. TKO showed significant decrease in phosphorylation of VEGFR-2 and Akt compared to WT under normoxic condition. We did not detect significant change in the activation of VEGFR2 and its downstream Akt in retinas from TKO and WT in response to hyperoxia. (*P

    Techniques Used: Activation Assay, Knock-Out, Mouse Assay

    Representative diagram shows the impact of TXNIP deletion on retina vasculature under both normoxia and hyperoxia. Under normoxia, retinas from TXNIP-deficient mice showed similar VEGF levels, less peroxynitrite (ONOO-) levels, less VEGF receptor-2 (pVEGFR2) activation and upregulated thioredoxin (Trx) that collectively lead to normal vascular development in comparison to WT mice. Under hyperoxia, retinas from WT mice showed higher peroxynitrite formation, less survival Akt activation (pAkt) and upregulated proapoptotic signal of ASK-1 resulting in vaso-obliteration. Retinas from TKO although showed less peroxynitrite levels and maintained Akt activation, retinas experienced significant decreases in thioredoxin (Trx) that shift the balance of the ASK-1-Trx inhibitory complex and increases the activation of the proapoptotic ASK-1 pathway leading to exacerbated vasoobliteration compared to WT.
    Figure Legend Snippet: Representative diagram shows the impact of TXNIP deletion on retina vasculature under both normoxia and hyperoxia. Under normoxia, retinas from TXNIP-deficient mice showed similar VEGF levels, less peroxynitrite (ONOO-) levels, less VEGF receptor-2 (pVEGFR2) activation and upregulated thioredoxin (Trx) that collectively lead to normal vascular development in comparison to WT mice. Under hyperoxia, retinas from WT mice showed higher peroxynitrite formation, less survival Akt activation (pAkt) and upregulated proapoptotic signal of ASK-1 resulting in vaso-obliteration. Retinas from TKO although showed less peroxynitrite levels and maintained Akt activation, retinas experienced significant decreases in thioredoxin (Trx) that shift the balance of the ASK-1-Trx inhibitory complex and increases the activation of the proapoptotic ASK-1 pathway leading to exacerbated vasoobliteration compared to WT.

    Techniques Used: Mouse Assay, Activation Assay

    5) Product Images from "The adaptor protein Shc integrates growth factor and ECM signaling during postnatal angiogenesis"

    Article Title: The adaptor protein Shc integrates growth factor and ECM signaling during postnatal angiogenesis

    Journal: Blood

    doi: 10.1182/blood-2011-10-384560

    Shc is required for VEGF-induced EC survival but not migration toward VEGF or proliferation. (A) HUVECs were serum starved for 24 hours with or without 100 ng/mL of VEGF to induce apoptosis. Lysates were immunoblotted for cleaved caspase 3 and GAPDH as a loading control. Survival was quantified by comparing the amount of cleaved caspase 3 present in lysate. Values shown are means ± SEM (n = 4 independent experiments). (B) Chemotaxis toward the VEGF gradient was measured using Boyden chambers containing 100 ng/mL of VEGF or vehicle in the lower well. After 4 hours of migration, cells that had migrated to the underside of the membrane were counted using an inverted microscope. Five random fields were imaged per filter. Values shown are means ± SEM (n = 3 independent experiments, 2 filters per condition per experiment). * P
    Figure Legend Snippet: Shc is required for VEGF-induced EC survival but not migration toward VEGF or proliferation. (A) HUVECs were serum starved for 24 hours with or without 100 ng/mL of VEGF to induce apoptosis. Lysates were immunoblotted for cleaved caspase 3 and GAPDH as a loading control. Survival was quantified by comparing the amount of cleaved caspase 3 present in lysate. Values shown are means ± SEM (n = 4 independent experiments). (B) Chemotaxis toward the VEGF gradient was measured using Boyden chambers containing 100 ng/mL of VEGF or vehicle in the lower well. After 4 hours of migration, cells that had migrated to the underside of the membrane were counted using an inverted microscope. Five random fields were imaged per filter. Values shown are means ± SEM (n = 3 independent experiments, 2 filters per condition per experiment). * P

    Techniques Used: Migration, Chemotaxis Assay, Inverted Microscopy

    Survival requires integration of VEGF and integrin signaling through Shc. (A) HUVECs were seeded on FN- or CL-coated dishes, and then serum starved for 24 hours with or without 100 ng/mL of VEGF to induce apoptosis. Lysates were immunoblotted for cleaved caspase 3 and GAPDH as a loading control. Survival was quantified by comparing the amount of cleaved caspase 3 present in lysate. Values shown are means ± SEM (n = 3 independent experiments).
    Figure Legend Snippet: Survival requires integration of VEGF and integrin signaling through Shc. (A) HUVECs were seeded on FN- or CL-coated dishes, and then serum starved for 24 hours with or without 100 ng/mL of VEGF to induce apoptosis. Lysates were immunoblotted for cleaved caspase 3 and GAPDH as a loading control. Survival was quantified by comparing the amount of cleaved caspase 3 present in lysate. Values shown are means ± SEM (n = 3 independent experiments).

    Techniques Used:

    6) Product Images from "CD45-CD14+CD34+ Murine Bone Marrow Low-Adherent Mesenchymal Primitive Cells Preserve Multilineage Differentiation Potential in Long-Term In Vitro Culture"

    Article Title: CD45-CD14+CD34+ Murine Bone Marrow Low-Adherent Mesenchymal Primitive Cells Preserve Multilineage Differentiation Potential in Long-Term In Vitro Culture

    Journal: Molecules and Cells

    doi: 10.1007/s10059-011-2176-y

    Tube formation on Matrigel. (A) Both non-differentiated and differentiated MSC (in EGM-2MV medium or DMEM with VEGF) efficiently formed tubes without the sphere formation step (magnification 100×). (B) Tube formation by MSC which undergo differentiation
    Figure Legend Snippet: Tube formation on Matrigel. (A) Both non-differentiated and differentiated MSC (in EGM-2MV medium or DMEM with VEGF) efficiently formed tubes without the sphere formation step (magnification 100×). (B) Tube formation by MSC which undergo differentiation

    Techniques Used:

    7) Product Images from "Regulated Splicing of the α6 Integrin Cytoplasmic Domain Determines the Fate of Breast Cancer Stem Cells"

    Article Title: Regulated Splicing of the α6 Integrin Cytoplasmic Domain Determines the Fate of Breast Cancer Stem Cells

    Journal: Cell reports

    doi: 10.1016/j.celrep.2014.03.059

    Identification of distinct CD44 high CD24 low populations that differ in morphology and stem cell properties A . MCF-10A ER/SRC cells were treated with 4-Hydroxy-Tamoxifen (TAM) and FACS analyzed using CD44, CD24 and α6 (GoH3) antibodies. B . The CD44 high /CD24 low population isolated from TAM-treated MCF-10A ER/SRC cells was sorted by FACS into two subpopulations based on expression of the α6 integrin subunit. Photomicrographs of these two subpopulations designated as EPTH (α6 high) and MES (α6 low) are shown. Scale bar = 100 μm C . Cell extracts from EPTH and MES cells were immunoblotted to assess expression of N-Cadherin, E-Cadherin, HIF-1α, vimentin, actin and VEGF-A (left panel). EPTH and MES cells were immunostained for CK8 and CK18 and the quantitation of positive cells is presented (Right panel). D . Expression of integrin α6, β1 and β4 mRNAs was quantified in EPTH and MES cells using qPCR. E . The CD44 high /CD24 low population from TAM treated MCF-10A ER/SRC cells was stained with PKH26 and cultured for 14 days. Cells were analyzed by FACS for PKH and integrin α6 expression. F . Expression of ALDH1A1 and BMI-1 mRNAs was quantified in EPTH and MES cells using qPCR. G The CD44 high /CD24 low population isolated from TAM-treated MCF-10A ER/SRC cells was treated with either taxol or Ethanol for 7 days and integrin α6 surface expression was analyzed by FACS. H . TAM- treated MCF-10A ER/SRC cells were FACS sorted into subpopulations based on expression of CD44 and CD24 and assayed for mammosphere formation (left panel). EPTH and MES cells were assayed for mammosphere formation (right panel). I . EPTH and MES cells (10 6 cells per mouse) were implanted in the mammary fat pads of NSG mice (n=12) and tumor formation was assessed by palpation. The curve comparison was done using Log-rank test (p=0.006).
    Figure Legend Snippet: Identification of distinct CD44 high CD24 low populations that differ in morphology and stem cell properties A . MCF-10A ER/SRC cells were treated with 4-Hydroxy-Tamoxifen (TAM) and FACS analyzed using CD44, CD24 and α6 (GoH3) antibodies. B . The CD44 high /CD24 low population isolated from TAM-treated MCF-10A ER/SRC cells was sorted by FACS into two subpopulations based on expression of the α6 integrin subunit. Photomicrographs of these two subpopulations designated as EPTH (α6 high) and MES (α6 low) are shown. Scale bar = 100 μm C . Cell extracts from EPTH and MES cells were immunoblotted to assess expression of N-Cadherin, E-Cadherin, HIF-1α, vimentin, actin and VEGF-A (left panel). EPTH and MES cells were immunostained for CK8 and CK18 and the quantitation of positive cells is presented (Right panel). D . Expression of integrin α6, β1 and β4 mRNAs was quantified in EPTH and MES cells using qPCR. E . The CD44 high /CD24 low population from TAM treated MCF-10A ER/SRC cells was stained with PKH26 and cultured for 14 days. Cells were analyzed by FACS for PKH and integrin α6 expression. F . Expression of ALDH1A1 and BMI-1 mRNAs was quantified in EPTH and MES cells using qPCR. G The CD44 high /CD24 low population isolated from TAM-treated MCF-10A ER/SRC cells was treated with either taxol or Ethanol for 7 days and integrin α6 surface expression was analyzed by FACS. H . TAM- treated MCF-10A ER/SRC cells were FACS sorted into subpopulations based on expression of CD44 and CD24 and assayed for mammosphere formation (left panel). EPTH and MES cells were assayed for mammosphere formation (right panel). I . EPTH and MES cells (10 6 cells per mouse) were implanted in the mammary fat pads of NSG mice (n=12) and tumor formation was assessed by palpation. The curve comparison was done using Log-rank test (p=0.006).

    Techniques Used: FACS, Isolation, Expressing, Quantitation Assay, Real-time Polymerase Chain Reaction, Staining, Cell Culture, Mouse Assay

    8) Product Images from "Morphological Plasticity of Emerging Purkinje Cells in Response to Exogenous VEGF"

    Article Title: Morphological Plasticity of Emerging Purkinje Cells in Response to Exogenous VEGF

    Journal: Frontiers in Molecular Neuroscience

    doi: 10.3389/fnmol.2017.00002

    Morphometric analysis of VEGF effects on neonatal PC dendrites. (A) Analysis of young, calbindin-stained PCs (labeled with green fluorescent secondary antibody, p1 + 5 div), and treated with VEGF (B) , axitinib (C) or VEGF + axtinib (D) for a period of 48 h. (E) Morphometric analysis of the dendritic length. Data are provided as means ± SEM. Data were tested for significance using one-way ANOVA with Bonferroni multiple comparisons post-test. Significant differences are indicated by *** p
    Figure Legend Snippet: Morphometric analysis of VEGF effects on neonatal PC dendrites. (A) Analysis of young, calbindin-stained PCs (labeled with green fluorescent secondary antibody, p1 + 5 div), and treated with VEGF (B) , axitinib (C) or VEGF + axtinib (D) for a period of 48 h. (E) Morphometric analysis of the dendritic length. Data are provided as means ± SEM. Data were tested for significance using one-way ANOVA with Bonferroni multiple comparisons post-test. Significant differences are indicated by *** p

    Techniques Used: Staining, Labeling

    Morphometric analysis of VEGF effects on mature PC dendrites and cell somata. Analysis of the total dendritic length (one dendrite is exemplarily labeled in red), circumference of the dendritic arbor and cell soma area (blue encircled) of pEYFP-actin microinjected PCs after a 48 h incubation time. (A) Untreated PC (p9 + 21 div) and the same PC after VEGF administration for 48 h (B) . (C) Changes of morphometric parameters for controls and treated cells are given in percent; data are provided as means ± SEM. Untreated neurons were defined as control and treated cells were normalized to this control. Data compared to control were tested for significance using Student’s t -test. n = 20; Scale bars: 50 μm.
    Figure Legend Snippet: Morphometric analysis of VEGF effects on mature PC dendrites and cell somata. Analysis of the total dendritic length (one dendrite is exemplarily labeled in red), circumference of the dendritic arbor and cell soma area (blue encircled) of pEYFP-actin microinjected PCs after a 48 h incubation time. (A) Untreated PC (p9 + 21 div) and the same PC after VEGF administration for 48 h (B) . (C) Changes of morphometric parameters for controls and treated cells are given in percent; data are provided as means ± SEM. Untreated neurons were defined as control and treated cells were normalized to this control. Data compared to control were tested for significance using Student’s t -test. n = 20; Scale bars: 50 μm.

    Techniques Used: Labeling, Incubation

    Morphometric analysis of VEGF effects on juvenile PC dendrites and cell somata. (A) Analysis of the total dendritic length of calbindin-stained PCs (red; p1 + 16 div), or PCs incubated with VEGF (B) , VEGF + axitinib or axitinib for a period of 48 h. (C) Morphometric analysis of the dendritic length. Data are provided as means ± SEM. Data were tested for significance using one-way ANOVA with Bonferroni multiple comparisons post-test. Significant differences are indicated by *** p
    Figure Legend Snippet: Morphometric analysis of VEGF effects on juvenile PC dendrites and cell somata. (A) Analysis of the total dendritic length of calbindin-stained PCs (red; p1 + 16 div), or PCs incubated with VEGF (B) , VEGF + axitinib or axitinib for a period of 48 h. (C) Morphometric analysis of the dendritic length. Data are provided as means ± SEM. Data were tested for significance using one-way ANOVA with Bonferroni multiple comparisons post-test. Significant differences are indicated by *** p

    Techniques Used: Staining, Incubation

    9) Product Images from "Effects of bone morphogenetic protein-2 (BMP-2) and vascular endothelial growth factor (VEGF) release from polylactide-poly (ethylene glycol)-polylactide (PELA) microcapsule-based scaffolds on bone"

    Article Title: Effects of bone morphogenetic protein-2 (BMP-2) and vascular endothelial growth factor (VEGF) release from polylactide-poly (ethylene glycol)-polylactide (PELA) microcapsule-based scaffolds on bone

    Journal: Brazilian Journal of Medical and Biological Research

    doi: 10.1590/1414-431X20176520

    Weight loss ( A ), swelling ratio ( B ) and cumulative release profile ( C ) of BMP-2/PELA/VEGF scaffolds in PBS at 37°C. Data are reported as means±SD. BMP-2: bone morphogenetic protein-2; PELA: polylactide-poly (ethylene glycol)-polylactide; VEGF: vascular endothelial growth factor; Ww: wet weight; Wd: dry weight.
    Figure Legend Snippet: Weight loss ( A ), swelling ratio ( B ) and cumulative release profile ( C ) of BMP-2/PELA/VEGF scaffolds in PBS at 37°C. Data are reported as means±SD. BMP-2: bone morphogenetic protein-2; PELA: polylactide-poly (ethylene glycol)-polylactide; VEGF: vascular endothelial growth factor; Ww: wet weight; Wd: dry weight.

    Techniques Used:

    Effects of BMP-2/PELA/VEGF scaffolds on the activation of mitogen-activated protein kinase (MAPK) signaling in rats mesenchymal stem cells. A , Expression of total and phosphorylated ERK1/2, JNKs, and p38 proteins. B , Contrast gray values corresponding to phosphorylated ERK1/2, JNKs, and p38 based on western blotting analysis. Results are reported as means±SD (n=5). *P
    Figure Legend Snippet: Effects of BMP-2/PELA/VEGF scaffolds on the activation of mitogen-activated protein kinase (MAPK) signaling in rats mesenchymal stem cells. A , Expression of total and phosphorylated ERK1/2, JNKs, and p38 proteins. B , Contrast gray values corresponding to phosphorylated ERK1/2, JNKs, and p38 based on western blotting analysis. Results are reported as means±SD (n=5). *P

    Techniques Used: Activation Assay, Expressing, Western Blot

    Expression of Wnt and β-catenin proteins in BMP-2/PELA/VEGF and BMP-2/PELA scaffolds, as well as the positive control. A , Western blotting images. B , Quantification of Wnt and β-catenin expression based on western blotting analysis. Results are reported as means±SD (n=5). *P
    Figure Legend Snippet: Expression of Wnt and β-catenin proteins in BMP-2/PELA/VEGF and BMP-2/PELA scaffolds, as well as the positive control. A , Western blotting images. B , Quantification of Wnt and β-catenin expression based on western blotting analysis. Results are reported as means±SD (n=5). *P

    Techniques Used: Expressing, Positive Control, Western Blot

    Results of the MTT assay after incubation of cells with PELA scaffolds. Cells cultured in the absence of scaffolds served as the positive control. Data are reported as means±SD. BMP-2: bone morphogenetic protein-2; PELA: polylactide-poly (ethylene glycol)-polylactide; VEGF: vascular endothelial growth factor.
    Figure Legend Snippet: Results of the MTT assay after incubation of cells with PELA scaffolds. Cells cultured in the absence of scaffolds served as the positive control. Data are reported as means±SD. BMP-2: bone morphogenetic protein-2; PELA: polylactide-poly (ethylene glycol)-polylactide; VEGF: vascular endothelial growth factor.

    Techniques Used: MTT Assay, Incubation, Cell Culture, Positive Control

    Expression of alkaline phosphatase (ALP) protein in BMP-2/PELA/VEGF and BMP-2/PELA scaffolds, as well as the positive control, 3, 7, and 14 days after mesenchymal stem cells seeding. A , Western blotting images. B , Quantification of ALP based on western blotting analysis. Results are reported as means±SD (n=5). *P
    Figure Legend Snippet: Expression of alkaline phosphatase (ALP) protein in BMP-2/PELA/VEGF and BMP-2/PELA scaffolds, as well as the positive control, 3, 7, and 14 days after mesenchymal stem cells seeding. A , Western blotting images. B , Quantification of ALP based on western blotting analysis. Results are reported as means±SD (n=5). *P

    Techniques Used: Expressing, ALP Assay, Positive Control, Western Blot

    Effects of BMP-2/PELA ( A ) and PELA/VEGF ( B ) scaffolds, as well as the positive control ( C ), on the activation of mitogen-activated protein kinase (MAPK) signaling in rBMSCs cells. Results are reported as means±SD.
    Figure Legend Snippet: Effects of BMP-2/PELA ( A ) and PELA/VEGF ( B ) scaffolds, as well as the positive control ( C ), on the activation of mitogen-activated protein kinase (MAPK) signaling in rBMSCs cells. Results are reported as means±SD.

    Techniques Used: Positive Control, Activation Assay

    10) Product Images from "Hyperglycemia induced testicular damage in type 2 diabetes mellitus rats exhibiting microcirculation impairments associated with vascular endothelial growth factor decreased via PI3K/Akt pathway"

    Article Title: Hyperglycemia induced testicular damage in type 2 diabetes mellitus rats exhibiting microcirculation impairments associated with vascular endothelial growth factor decreased via PI3K/Akt pathway

    Journal: Oncotarget

    doi: 10.18632/oncotarget.23915

    The change of serum glucose and body weights Serum glucose (A) and body weights (B) in diabetes rats compared to control group and diabetes +VEGF group. Diabetes group and diabetes + VEGF group were intraperitoneally injected with STZ at week8. From week 9, diabetes + VEGF group was daily treatment with VEGF. +* P
    Figure Legend Snippet: The change of serum glucose and body weights Serum glucose (A) and body weights (B) in diabetes rats compared to control group and diabetes +VEGF group. Diabetes group and diabetes + VEGF group were intraperitoneally injected with STZ at week8. From week 9, diabetes + VEGF group was daily treatment with VEGF. +* P

    Techniques Used: Injection

    11) Product Images from "Deletion of p75NTR prevents vaso-obliteration and retinal neovascularization via activation of Trk- A receptor in ischemic retinopathy model"

    Article Title: Deletion of p75NTR prevents vaso-obliteration and retinal neovascularization via activation of Trk- A receptor in ischemic retinopathy model

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-30029-0

    Deletion of p75 NTR preserved hypoxia-induced VEGF expression and VEGFR2 activation. ( A ) Representative Western blotting and bar graph of retinal VEGF protein expression from WT and p75 NTR−/− pups exposed to OIR at p14. Two-way ANOVA showed significant effect of hypoxia increasing VEGF both in WT and p75 NTR−/− pups (*significant compared to WT normoxic group, p
    Figure Legend Snippet: Deletion of p75 NTR preserved hypoxia-induced VEGF expression and VEGFR2 activation. ( A ) Representative Western blotting and bar graph of retinal VEGF protein expression from WT and p75 NTR−/− pups exposed to OIR at p14. Two-way ANOVA showed significant effect of hypoxia increasing VEGF both in WT and p75 NTR−/− pups (*significant compared to WT normoxic group, p

    Techniques Used: Expressing, Activation Assay, Western Blot

    12) Product Images from "Characterization of Oral Immunity in Cases and Close Household Contacts Exposed to Andes Orthohantavirus (ANDV)"

    Article Title: Characterization of Oral Immunity in Cases and Close Household Contacts Exposed to Andes Orthohantavirus (ANDV)

    Journal: Frontiers in Cellular and Infection Microbiology

    doi: 10.3389/fcimb.2020.557273

    Comparison of concentration of different cytokines in four ANDV-infected cases in acute stage and convalescent stage. Concentrations are represented in pg/mL of INFγ, IL10, IL12p70, IL1β, IL6, IL8, IP10, TNFα, and VEGF. Clear boxes represent values in acute stage and dark boxes values in convalescent stage; whiskers represent minimum and maximum values and horizontal bars in the box the median value (Wilcoxon rank test, p
    Figure Legend Snippet: Comparison of concentration of different cytokines in four ANDV-infected cases in acute stage and convalescent stage. Concentrations are represented in pg/mL of INFγ, IL10, IL12p70, IL1β, IL6, IL8, IP10, TNFα, and VEGF. Clear boxes represent values in acute stage and dark boxes values in convalescent stage; whiskers represent minimum and maximum values and horizontal bars in the box the median value (Wilcoxon rank test, p

    Techniques Used: Concentration Assay, Infection

    Comparison of the concentration (pg/mL) of different factors measured in saliva between ANDV-infected cases, close household contacts and healthy controls not exposed. (A) Quantification (pg/mL) of INFγ, IL10, IL12p70, IL1β, IL6, IL8, IP10, TNFα, and VEGF in all groups; dark boxes represent ANDV-infected cases, clear boxes represent close household contacts, and gray boxes represent healthy controls not exposed; Boxes represent median values and bars interquartile range. Comparisons are significance between columns: ***All group are statistically significant, **a: all group are statistically significant, except for Healthy controls not exposed and Close household contact, *b: only between Cases and Healthy controls not exposed is statistically significant, *c: only between Cases and Close household contact is statistically significant (Kruskal-Wallis test and Mann Whitney test, p
    Figure Legend Snippet: Comparison of the concentration (pg/mL) of different factors measured in saliva between ANDV-infected cases, close household contacts and healthy controls not exposed. (A) Quantification (pg/mL) of INFγ, IL10, IL12p70, IL1β, IL6, IL8, IP10, TNFα, and VEGF in all groups; dark boxes represent ANDV-infected cases, clear boxes represent close household contacts, and gray boxes represent healthy controls not exposed; Boxes represent median values and bars interquartile range. Comparisons are significance between columns: ***All group are statistically significant, **a: all group are statistically significant, except for Healthy controls not exposed and Close household contact, *b: only between Cases and Healthy controls not exposed is statistically significant, *c: only between Cases and Close household contact is statistically significant (Kruskal-Wallis test and Mann Whitney test, p

    Techniques Used: Concentration Assay, Infection, MANN-WHITNEY

    Heatmap showing the cytokine response to ANDV infection in 33 ANDV-infected cases in saliva and serum samples concomitantly taken. The heatmap was constructed in Heatmapper ( www.heatmapper.ca ; Babicki et al., 2016 ) according to the fold increase of each cytokine (INFγ, IL10, IL12p70, IL1β, IL6, IL8, IP10, TNFα, and VEGF) concentration of 33 ANDV-infected patients normalized against the median concentration of healthy subjects. Columns represent the Z-scored data for each patient split into two compartments, saliva (S) and serum (B). Rows represents each individual (from 1 to 33) according to days since the onset of symptoms. Colors indicate deviations from the mean of zero (white), as indicated in the color key (Z-score−4 blue, and 4 yellow).
    Figure Legend Snippet: Heatmap showing the cytokine response to ANDV infection in 33 ANDV-infected cases in saliva and serum samples concomitantly taken. The heatmap was constructed in Heatmapper ( www.heatmapper.ca ; Babicki et al., 2016 ) according to the fold increase of each cytokine (INFγ, IL10, IL12p70, IL1β, IL6, IL8, IP10, TNFα, and VEGF) concentration of 33 ANDV-infected patients normalized against the median concentration of healthy subjects. Columns represent the Z-scored data for each patient split into two compartments, saliva (S) and serum (B). Rows represents each individual (from 1 to 33) according to days since the onset of symptoms. Colors indicate deviations from the mean of zero (white), as indicated in the color key (Z-score−4 blue, and 4 yellow).

    Techniques Used: Infection, Construct, Concentration Assay

    13) Product Images from "Is Asthma Related to Choroidal Neovascularization?"

    Article Title: Is Asthma Related to Choroidal Neovascularization?

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0035415

    Western blot of C3 and VEGF. Western blot showing C3α’-chain, C3α-chain and VEGF expression in the RPE/choroid layer of rats without asthma, rats with asthma and rats with asthma treated with compstatin 14 days after laser photocoagulation. This experiment was repeated three times.
    Figure Legend Snippet: Western blot of C3 and VEGF. Western blot showing C3α’-chain, C3α-chain and VEGF expression in the RPE/choroid layer of rats without asthma, rats with asthma and rats with asthma treated with compstatin 14 days after laser photocoagulation. This experiment was repeated three times.

    Techniques Used: Western Blot, Expressing

    14) Product Images from "Aging-related Decrease of Human ASC Angiogenic Potential Is Reversed by Hypoxia Preconditioning Through ROS Production"

    Article Title: Aging-related Decrease of Human ASC Angiogenic Potential Is Reversed by Hypoxia Preconditioning Through ROS Production

    Journal: Molecular Therapy

    doi: 10.1038/mt.2012.213

    Hypoxia-preconditioning effect on in vitro redox metabolism and paracrine activity of hASC . hASC from donors aged 20–35 years and over 50 years were cultured in 0.5% O 2 for 24 hours before the measurement of ( a ) ROS production, ( b ) catalase, and ( c ) glutathione peroxidase activities as well as ( d ) VEGF secretion in the culture medium, n = 3–5. * P ≤ 0.05 and *** P ≤ 0.001 in normoxia versus hypoxia culture conditions and # P ≤ 0.05 in young versus old donor groups in hypoxia culture condition. hASC, human adipose-derived stromal cell; ns, not significant; ROS, reactive oxygen species; VEGF, vascular endothelial growth factor.
    Figure Legend Snippet: Hypoxia-preconditioning effect on in vitro redox metabolism and paracrine activity of hASC . hASC from donors aged 20–35 years and over 50 years were cultured in 0.5% O 2 for 24 hours before the measurement of ( a ) ROS production, ( b ) catalase, and ( c ) glutathione peroxidase activities as well as ( d ) VEGF secretion in the culture medium, n = 3–5. * P ≤ 0.05 and *** P ≤ 0.001 in normoxia versus hypoxia culture conditions and # P ≤ 0.05 in young versus old donor groups in hypoxia culture condition. hASC, human adipose-derived stromal cell; ns, not significant; ROS, reactive oxygen species; VEGF, vascular endothelial growth factor.

    Techniques Used: In Vitro, Activity Assay, Cell Culture, Derivative Assay

    Reversal effect of antioxidant treatment on capacities of hypoxic-preconditioned hASC from older donors . hASC from donors over 50 years old were simultaneously incubated at 0.5% O 2 and treated with NAC. After 24 hours, ( a ) ROS production and ( b ) VEGF secretion were assessed. Transplantation of 1 × 10 6 hypoxia-preconditioned hASC treated or not with NAC were intramuscularly injected in the ischemic hindlimb. ( c ) Representative photomicrographs of laser Doppler perfusion imaging and the ( d ) quantitative evaluation of cutaneous blood flow in preserved limb, 14 days after treatment are presented. Cutaneous blood flow is expressed as the percentage normalized to control of the ratio ischemic leg perfusion/nonischemic leg perfusion (I/NI), n = 1–5 independent experiments. * P ≤ 0.05 and ** P ≤ 0.01 in normoxia versus hypoxia or hypoxia + NAC culture conditions. §§ P ≤ 0.01 in hypoxia-preconditioning culture condition, in the presence versus the absence of NAC. hASC, human adipose-derived stromal cell; NAC, N-acetylcysteine; ROS, reactive oxygen species; VEGF, vascular endothelial growth factor.
    Figure Legend Snippet: Reversal effect of antioxidant treatment on capacities of hypoxic-preconditioned hASC from older donors . hASC from donors over 50 years old were simultaneously incubated at 0.5% O 2 and treated with NAC. After 24 hours, ( a ) ROS production and ( b ) VEGF secretion were assessed. Transplantation of 1 × 10 6 hypoxia-preconditioned hASC treated or not with NAC were intramuscularly injected in the ischemic hindlimb. ( c ) Representative photomicrographs of laser Doppler perfusion imaging and the ( d ) quantitative evaluation of cutaneous blood flow in preserved limb, 14 days after treatment are presented. Cutaneous blood flow is expressed as the percentage normalized to control of the ratio ischemic leg perfusion/nonischemic leg perfusion (I/NI), n = 1–5 independent experiments. * P ≤ 0.05 and ** P ≤ 0.01 in normoxia versus hypoxia or hypoxia + NAC culture conditions. §§ P ≤ 0.01 in hypoxia-preconditioning culture condition, in the presence versus the absence of NAC. hASC, human adipose-derived stromal cell; NAC, N-acetylcysteine; ROS, reactive oxygen species; VEGF, vascular endothelial growth factor.

    Techniques Used: Incubation, Transplantation Assay, Injection, Imaging, Flow Cytometry, Derivative Assay

    Effect of aging on in vitro endothelial differentiation and paracrine activity of hASC . ( a ) hASC were cultured in control or angiogenic medium and for immunostaining of CD31+ differentiated cells forming highly branched networks (green) and nuclei staining with DAPI (blue). Bar = 100 µm. Representative fluorescence microscopy was used for the ( b ) CD31 network length measurement and ( c ) cell number counting, n = 13. * P ≤ 0.05 in control medium versus angiogenic medium. ( d ) Proangiogenic and pro-survival growth factors or ( f ) cytokines mRNA expression contents as well as ( e ) human protein secretion were measured in cultured hASC, n = 7–9. # P ≤ 0.05 in young versus old donors groups. DAPI, 4′,6-diamidino-2-phenylindole; hASC, human adipose-derived stromal cell; HGF, hepatocyte growth factor; IGF, insulin-like growth factor; IL, interleukin; ns, not significant; TGF-β, transforming growth factor-β TNF-α, tumor necrosis factor-α VEGF, vascular endothelial growth factor.
    Figure Legend Snippet: Effect of aging on in vitro endothelial differentiation and paracrine activity of hASC . ( a ) hASC were cultured in control or angiogenic medium and for immunostaining of CD31+ differentiated cells forming highly branched networks (green) and nuclei staining with DAPI (blue). Bar = 100 µm. Representative fluorescence microscopy was used for the ( b ) CD31 network length measurement and ( c ) cell number counting, n = 13. * P ≤ 0.05 in control medium versus angiogenic medium. ( d ) Proangiogenic and pro-survival growth factors or ( f ) cytokines mRNA expression contents as well as ( e ) human protein secretion were measured in cultured hASC, n = 7–9. # P ≤ 0.05 in young versus old donors groups. DAPI, 4′,6-diamidino-2-phenylindole; hASC, human adipose-derived stromal cell; HGF, hepatocyte growth factor; IGF, insulin-like growth factor; IL, interleukin; ns, not significant; TGF-β, transforming growth factor-β TNF-α, tumor necrosis factor-α VEGF, vascular endothelial growth factor.

    Techniques Used: In Vitro, Activity Assay, Cell Culture, Immunostaining, Staining, Fluorescence, Microscopy, Expressing, Derivative Assay

    15) Product Images from "Schwann-like cells seeded in acellular nerve grafts improve nerve regeneration"

    Article Title: Schwann-like cells seeded in acellular nerve grafts improve nerve regeneration

    Journal: BMC Musculoskeletal Disorders

    doi: 10.1186/1471-2474-15-165

    S-100 and VEGF immunostaining and IOD value analyses at 12 weeks postoperatively. S-100 immunostaining ( A-C , scale bar = 10 μm) and VEGF immunostaining ( D-F , scale bar = 20 μm) at 12 weeks postoperatively with SLCs (A and D) , BM-MSCs (B and E) and isografts (C and F) . The IOD values of the positive expression of S-100 and VEGF in the regenerated nerves (G) . The isograft and ANG + SLC groups showed a significantly higher level in both S-100 and VEGF immunostaining compared with the ANG + BM-MSC group. The data were shown as the mean ± SEM. * P
    Figure Legend Snippet: S-100 and VEGF immunostaining and IOD value analyses at 12 weeks postoperatively. S-100 immunostaining ( A-C , scale bar = 10 μm) and VEGF immunostaining ( D-F , scale bar = 20 μm) at 12 weeks postoperatively with SLCs (A and D) , BM-MSCs (B and E) and isografts (C and F) . The IOD values of the positive expression of S-100 and VEGF in the regenerated nerves (G) . The isograft and ANG + SLC groups showed a significantly higher level in both S-100 and VEGF immunostaining compared with the ANG + BM-MSC group. The data were shown as the mean ± SEM. * P

    Techniques Used: Immunostaining, Expressing

    16) Product Images from "TDP-43 and FUS RNA-binding Proteins Bind Distinct Sets of Cytoplasmic Messenger RNAs and Differently Regulate Their Post-transcriptional Fate in Motoneuron-like Cells *"

    Article Title: TDP-43 and FUS RNA-binding Proteins Bind Distinct Sets of Cytoplasmic Messenger RNAs and Differently Regulate Their Post-transcriptional Fate in Motoneuron-like Cells *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M111.333450

    Modulation of TDP-43 influences PGRN protein content. A , shown is a representative Western blot of VEGF and PGRN in mock- and FLAG-hTDP-43-transfected NSC-34 cells ( left ) and densitometric analysis (mean ± S.E.; n = 4; paired t test analysis;
    Figure Legend Snippet: Modulation of TDP-43 influences PGRN protein content. A , shown is a representative Western blot of VEGF and PGRN in mock- and FLAG-hTDP-43-transfected NSC-34 cells ( left ) and densitometric analysis (mean ± S.E.; n = 4; paired t test analysis;

    Techniques Used: Western Blot, Transfection

    Effect of TDP-43 on the translatability of Vegfa and Grn mRNAs. A , shown is a representative Western blot of VEGF and PGRN in cell lysates of siCTRL and siTDP-43 NSC-34 cells (96-h silencing) ( left ). α-Tubulin (α -Tub ) was used for sample
    Figure Legend Snippet: Effect of TDP-43 on the translatability of Vegfa and Grn mRNAs. A , shown is a representative Western blot of VEGF and PGRN in cell lysates of siCTRL and siTDP-43 NSC-34 cells (96-h silencing) ( left ). α-Tubulin (α -Tub ) was used for sample

    Techniques Used: Western Blot

    17) Product Images from "Mesenchymal stem cells overexpressing PEDF decrease the angiogenesis of gliomas"

    Article Title: Mesenchymal stem cells overexpressing PEDF decrease the angiogenesis of gliomas

    Journal: Bioscience Reports

    doi: 10.1042/BSR20110124

    Migration pattern of MSCs and fibroblast in vitro Compared with the PBS, U87cells and VEGF led to a distinct increase of MSCs migration. The PEDF, however, showed an inhibitory effect on MSCs. Compared with fibroblasts, MSCs possess greater migratory capacity than fibroblasts under the stimulation of VEGF or cultured U87 cells (* P
    Figure Legend Snippet: Migration pattern of MSCs and fibroblast in vitro Compared with the PBS, U87cells and VEGF led to a distinct increase of MSCs migration. The PEDF, however, showed an inhibitory effect on MSCs. Compared with fibroblasts, MSCs possess greater migratory capacity than fibroblasts under the stimulation of VEGF or cultured U87 cells (* P

    Techniques Used: Migration, In Vitro, Cell Culture

    18) Product Images from "Identification of a Role for the PI3K/AKT/mTOR Signaling Pathway in Innate Immune Cells"

    Article Title: Identification of a Role for the PI3K/AKT/mTOR Signaling Pathway in Innate Immune Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0094496

    The PI3K inhibitor LY suppresses the secretion of proinflammatory cytokines from monocytes and macrophages. (A) Diagram of Luminex based multiplex assays. Antibodies against cytokines were conjugated with different color-coded beads to capture the analytes, and biotinylated detection antibodies and Streptavidin R-Phycoerythrin Conjugate (SAPE) were then added sequentially to bind the captured analytes. The mixture was analyzed with Luminex 200 instrument, whereby the bead set is distinguished by a red laser and the PE signal on the bead is determined by a green laser. (B) Standard curve determination of G-CSF, IL-6, TNF-α, and VEGF. (C–F) Analysis of proinflammatory cytokines from THP-1 monocytes and THP-1 derived macrophages. a indicates P
    Figure Legend Snippet: The PI3K inhibitor LY suppresses the secretion of proinflammatory cytokines from monocytes and macrophages. (A) Diagram of Luminex based multiplex assays. Antibodies against cytokines were conjugated with different color-coded beads to capture the analytes, and biotinylated detection antibodies and Streptavidin R-Phycoerythrin Conjugate (SAPE) were then added sequentially to bind the captured analytes. The mixture was analyzed with Luminex 200 instrument, whereby the bead set is distinguished by a red laser and the PE signal on the bead is determined by a green laser. (B) Standard curve determination of G-CSF, IL-6, TNF-α, and VEGF. (C–F) Analysis of proinflammatory cytokines from THP-1 monocytes and THP-1 derived macrophages. a indicates P

    Techniques Used: Luminex, Multiplex Assay, Derivative Assay

    19) Product Images from "Sequential Delivery of Cryogel Released Growth Factors and Cytokines Accelerates Wound Healing and Improves Tissue Regeneration"

    Article Title: Sequential Delivery of Cryogel Released Growth Factors and Cytokines Accelerates Wound Healing and Improves Tissue Regeneration

    Journal: Frontiers in Bioengineering and Biotechnology

    doi: 10.3389/fbioe.2020.00345

    Wound healing after treatment with cryogel. After total skin excision in mice, an internal splint model was performed, and the mice were divided into four groups by wound treatment: treated with cryogel alone, cryogel plus IL-10/TGF-β, cryogel plus VEGF/FGF, and cryogel plus all growth factors/cytokines (GF/C). Changes in wound area (% vs. day 0) over time are shown. Wound areas in the group with cryogel plus GF/C significantly decreased on days 7 and 10 as compared to the other groups. Values: mean ± SE. *** P
    Figure Legend Snippet: Wound healing after treatment with cryogel. After total skin excision in mice, an internal splint model was performed, and the mice were divided into four groups by wound treatment: treated with cryogel alone, cryogel plus IL-10/TGF-β, cryogel plus VEGF/FGF, and cryogel plus all growth factors/cytokines (GF/C). Changes in wound area (% vs. day 0) over time are shown. Wound areas in the group with cryogel plus GF/C significantly decreased on days 7 and 10 as compared to the other groups. Values: mean ± SE. *** P

    Techniques Used: Mouse Assay

    Biological activity of growth factors released from the cryogel. (A) Inhibition of mouse mammary gland cell line (NMuMG) proliferation by the cryogel released TGF-β, (B) Stimulation of mouse mast cell line (MC/9) proliferation by the cryogel released IL-10, (C) Stimulation of human umbilical vein endothelial cells (HUVEC) proliferation by the cryogel released VEGF, (D) Decrease in the wound area by the cryogel released FGF. (E) Representative images of wound areas quantified in (D) . Data were analyzed using one-way ANOVA with Bonferroni’s multiple comparisons test. ** P
    Figure Legend Snippet: Biological activity of growth factors released from the cryogel. (A) Inhibition of mouse mammary gland cell line (NMuMG) proliferation by the cryogel released TGF-β, (B) Stimulation of mouse mast cell line (MC/9) proliferation by the cryogel released IL-10, (C) Stimulation of human umbilical vein endothelial cells (HUVEC) proliferation by the cryogel released VEGF, (D) Decrease in the wound area by the cryogel released FGF. (E) Representative images of wound areas quantified in (D) . Data were analyzed using one-way ANOVA with Bonferroni’s multiple comparisons test. ** P

    Techniques Used: Activity Assay, Inhibition

    In vitro cumulative release of growth factors. Indicated concentrations of TGF-β, IL-10, VEGF, and FGF were incorporated into the cryogel. The concentrations of released growth factors in the solution were measured by ELISA at 1, 3, 5, 7, and 10 days after factor incorporation into the cryogel.
    Figure Legend Snippet: In vitro cumulative release of growth factors. Indicated concentrations of TGF-β, IL-10, VEGF, and FGF were incorporated into the cryogel. The concentrations of released growth factors in the solution were measured by ELISA at 1, 3, 5, 7, and 10 days after factor incorporation into the cryogel.

    Techniques Used: In Vitro, Enzyme-linked Immunosorbent Assay

    20) Product Images from "Human Apolipoprotein(a) Kringle V Inhibits Ischemia-Induced Retinal Neovascularization via Suppression of Fibronectin-Mediated Angiogenesis"

    Article Title: Human Apolipoprotein(a) Kringle V Inhibits Ischemia-Induced Retinal Neovascularization via Suppression of Fibronectin-Mediated Angiogenesis

    Journal: Diabetes

    doi: 10.2337/db11-1541

    rhLK8 inhibits in vitro tube formation and migration of endothelial cells. We performed in vitro angiogenesis assays, tube formation, and wound migration assays to investigate the inhibitory effect of rhLK8 on the process of angiogenesis. A : Tube formation was quantified by counting the number of connected cells in randomly selected fields (original magnification ×200) via the light microscope and dividing the number by the total number of cells in each field. rhLK8 effectively reduced the degree of tube formation stimulated by VEGF in a dose-dependent manner. B : To assess the inhibitory effect of rhLK8 on migration of endothelial cells, HUVECs were cultured on the gelatin-coated dishes at 90% confluence and wounded with a blade. The degree of migration was quantified by counting the cells that migrated beyond the reference line in randomly selected fields (original magnification ×200). rhLK8 suppressed migration of endothelial cells stimulated by VEGF. Each experiment was repeated at least three times, and the data are presented as mean ± SD. * P
    Figure Legend Snippet: rhLK8 inhibits in vitro tube formation and migration of endothelial cells. We performed in vitro angiogenesis assays, tube formation, and wound migration assays to investigate the inhibitory effect of rhLK8 on the process of angiogenesis. A : Tube formation was quantified by counting the number of connected cells in randomly selected fields (original magnification ×200) via the light microscope and dividing the number by the total number of cells in each field. rhLK8 effectively reduced the degree of tube formation stimulated by VEGF in a dose-dependent manner. B : To assess the inhibitory effect of rhLK8 on migration of endothelial cells, HUVECs were cultured on the gelatin-coated dishes at 90% confluence and wounded with a blade. The degree of migration was quantified by counting the cells that migrated beyond the reference line in randomly selected fields (original magnification ×200). rhLK8 suppressed migration of endothelial cells stimulated by VEGF. Each experiment was repeated at least three times, and the data are presented as mean ± SD. * P

    Techniques Used: In Vitro, Migration, Light Microscopy, Cell Culture

    21) Product Images from "Erythropoietin Improves the Survival of Fat Tissue after Its Transplantation in Nude Mice"

    Article Title: Erythropoietin Improves the Survival of Fat Tissue after Its Transplantation in Nude Mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0013986

    Effect of EPO on the expression levels of angiogenic growth factors in the fat grafts. The fat grafts from the three different groups of mice were treated with either PBS (100 µl), 20 IU EPO/100 µl PBS (low-dose), or 100 IU EPO/100 µl PBS (high-dose) on the day of the fat injection, and the treatments were repeated every three days for 18 days. (A) Representative histological micrographs of PBS-, and low-dose- and high-dose-EPO treated fat grafts (left to right) presenting VEGF expression (upper panel), VEGFR-2 expression (middle panel), and EPOR expression (lower panel). (B) Representative western blots of the expression levels of the angiogenic factors in the PBS- and EPO-treated fat grafts at the end of the 15-week study period. bFGF: basic fibroblast growth factor; IGF-1: insulin-like growth factor-1; PDGF-BB: platelet-derived growth factor-BB; MMP-2: matrix metalloproteinase-2; PKB: protein kinase B; phosphoPKB: phosphorylated PKB. (C) Graphs representing the mean VEGF content (left), the mean VEGFR-2 expression (middle) and the mean EPOR expression (right) ± SD in the fat grafts in each treatment group. (D) The correlation between VEGF and MVD (left), and between mean VEGFR-2 (middle) and EPOR (right) expression and mean MVD in each group. * P
    Figure Legend Snippet: Effect of EPO on the expression levels of angiogenic growth factors in the fat grafts. The fat grafts from the three different groups of mice were treated with either PBS (100 µl), 20 IU EPO/100 µl PBS (low-dose), or 100 IU EPO/100 µl PBS (high-dose) on the day of the fat injection, and the treatments were repeated every three days for 18 days. (A) Representative histological micrographs of PBS-, and low-dose- and high-dose-EPO treated fat grafts (left to right) presenting VEGF expression (upper panel), VEGFR-2 expression (middle panel), and EPOR expression (lower panel). (B) Representative western blots of the expression levels of the angiogenic factors in the PBS- and EPO-treated fat grafts at the end of the 15-week study period. bFGF: basic fibroblast growth factor; IGF-1: insulin-like growth factor-1; PDGF-BB: platelet-derived growth factor-BB; MMP-2: matrix metalloproteinase-2; PKB: protein kinase B; phosphoPKB: phosphorylated PKB. (C) Graphs representing the mean VEGF content (left), the mean VEGFR-2 expression (middle) and the mean EPOR expression (right) ± SD in the fat grafts in each treatment group. (D) The correlation between VEGF and MVD (left), and between mean VEGFR-2 (middle) and EPOR (right) expression and mean MVD in each group. * P

    Techniques Used: Expressing, Mouse Assay, Injection, Western Blot, Derivative Assay

    Effect of VEGF on MVD and the extent of apoptosis in the fat grafts. PBS (100 µl) or VEGF (200 ng VEGF/100 µl PBS) were injected into the fat grafts in two different groups of mice on the day of the fat injection and every three days for 18 days. (A) Each bar represents the mean MVD ± SD from five regions of interest in each slide that was prepared from the harvested fat grafts of each treatment group at the end of the 15-week study period. (B) Each bar represents the mean VEGF content ± SD in the harvested fat grafts in each treatment group at the end of the 15-week study period. (C) The extent of apoptosis was measured by the TUNEL assay, and is expressed as a percentage of the extent of apoptosis in the PBS-treated fat grafts. Each bar represents the mean extent of apoptosis ± SD in the fat graft in each treatment group at the end of the 15-week study period. ** P
    Figure Legend Snippet: Effect of VEGF on MVD and the extent of apoptosis in the fat grafts. PBS (100 µl) or VEGF (200 ng VEGF/100 µl PBS) were injected into the fat grafts in two different groups of mice on the day of the fat injection and every three days for 18 days. (A) Each bar represents the mean MVD ± SD from five regions of interest in each slide that was prepared from the harvested fat grafts of each treatment group at the end of the 15-week study period. (B) Each bar represents the mean VEGF content ± SD in the harvested fat grafts in each treatment group at the end of the 15-week study period. (C) The extent of apoptosis was measured by the TUNEL assay, and is expressed as a percentage of the extent of apoptosis in the PBS-treated fat grafts. Each bar represents the mean extent of apoptosis ± SD in the fat graft in each treatment group at the end of the 15-week study period. ** P

    Techniques Used: Injection, Mouse Assay, TUNEL Assay

    22) Product Images from "On-Chip Synthesis of RNA Aptamer Microarrays for Multiplexed Protein Biosensing with SPR Imaging Measurements"

    Article Title: On-Chip Synthesis of RNA Aptamer Microarrays for Multiplexed Protein Biosensing with SPR Imaging Measurements

    Journal: Langmuir

    doi: 10.1021/la300656c

    SPRI difference images after sequential injection of (a) 40 nM VEGF and (b) 25 nM hTh for ten minutes, respectively. (c) Schematic of surface patterning of the microarray for multiplexed protein detection. Generator, detector element for VEGF and hTh, and Control elements are represented as G (a mixture of sequences G1 and G2), D1, D2, and C2. (d) Line profiles of VEGF (red) and hTh (black) obtained by the corresponding difference images shown in (a) and (b). Line profiles for VEGF contains D2 and C2, and that for hTh contains G and D1, confirming very little non-specific binding.
    Figure Legend Snippet: SPRI difference images after sequential injection of (a) 40 nM VEGF and (b) 25 nM hTh for ten minutes, respectively. (c) Schematic of surface patterning of the microarray for multiplexed protein detection. Generator, detector element for VEGF and hTh, and Control elements are represented as G (a mixture of sequences G1 and G2), D1, D2, and C2. (d) Line profiles of VEGF (red) and hTh (black) obtained by the corresponding difference images shown in (a) and (b). Line profiles for VEGF contains D2 and C2, and that for hTh contains G and D1, confirming very little non-specific binding.

    Techniques Used: Injection, Microarray, Binding Assay

    23) Product Images from "Cordycepin Suppresses Endothelial Cell Proliferation, Migration, Angiogenesis, and Tumor Growth by Regulating Focal Adhesion Kinase and p53"

    Article Title: Cordycepin Suppresses Endothelial Cell Proliferation, Migration, Angiogenesis, and Tumor Growth by Regulating Focal Adhesion Kinase and p53

    Journal: Cancers

    doi: 10.3390/cancers11020168

    Suppression of tube formation and in vivo angiogenesis by cordycepin. ( A ) HUVECs were treated with cordycepin for 48 h and seeded onto Matrigel-coated plates with 0–25 μg/mL cordycepin in M200 medium for another 6 h. Tube formation was examined by counting the number of branches. ( B ) Matrigel plug assay was performed to assess in vivo angiogenesis formation in C57BL/6 mice. The mice were implanted with Matrigel plugs containing vascular endothelial growth factor (VEGF) and heparin with or without 25 μg/mL cordycepin for seven days. The Matrigel plugs were harvested, and in vivo angiogenesis was evaluated by measuring the concentration of hemoglobin. Scale bars: mean ± SD. *, p
    Figure Legend Snippet: Suppression of tube formation and in vivo angiogenesis by cordycepin. ( A ) HUVECs were treated with cordycepin for 48 h and seeded onto Matrigel-coated plates with 0–25 μg/mL cordycepin in M200 medium for another 6 h. Tube formation was examined by counting the number of branches. ( B ) Matrigel plug assay was performed to assess in vivo angiogenesis formation in C57BL/6 mice. The mice were implanted with Matrigel plugs containing vascular endothelial growth factor (VEGF) and heparin with or without 25 μg/mL cordycepin for seven days. The Matrigel plugs were harvested, and in vivo angiogenesis was evaluated by measuring the concentration of hemoglobin. Scale bars: mean ± SD. *, p

    Techniques Used: In Vivo, Matrigel Assay, Mouse Assay, Concentration Assay

    24) Product Images from "Amentoflavone Inhibits Hepatocellular Carcinoma Progression Through Blockage of ERK/NF-ĸB Activation"

    Article Title: Amentoflavone Inhibits Hepatocellular Carcinoma Progression Through Blockage of ERK/NF-ĸB Activation

    Journal: In Vivo

    doi: 10.21873/invivo.11351

    Effect of amentoflavone on tumor progression-associated proteins modulated by extracellular signal-regulated kinase (ERK)/nuclear factorĸB (NF-ĸB) in SK-Hep1/luc2 tumor-bearing mice. Protein levels of phosphorylated (P)ERK, NF-ĸB p65 (Ser536), matrix metallopeptidase 9 (MMP- 9), vascular endothelial growth factor (VEGF), cyclin-D1, myeloid leukemia cell differentiation protein (MCL-1), cellular FADD-like IL-1β-converting enzyme-inhibitory protein (C-FLIP), and X-linked inhibitor of apoptosis protein (XIAP) in tumor tissues were investigated by immunohistochemistry. A: Image at magnification of 100×. B: Quantification of protein level. C: Pathological examination of liver tissues obtained from mice sacrificed on day 14 after treatment was evaluated by hematoxylin-eosin staining. aSignificantly different at p
    Figure Legend Snippet: Effect of amentoflavone on tumor progression-associated proteins modulated by extracellular signal-regulated kinase (ERK)/nuclear factorĸB (NF-ĸB) in SK-Hep1/luc2 tumor-bearing mice. Protein levels of phosphorylated (P)ERK, NF-ĸB p65 (Ser536), matrix metallopeptidase 9 (MMP- 9), vascular endothelial growth factor (VEGF), cyclin-D1, myeloid leukemia cell differentiation protein (MCL-1), cellular FADD-like IL-1β-converting enzyme-inhibitory protein (C-FLIP), and X-linked inhibitor of apoptosis protein (XIAP) in tumor tissues were investigated by immunohistochemistry. A: Image at magnification of 100×. B: Quantification of protein level. C: Pathological examination of liver tissues obtained from mice sacrificed on day 14 after treatment was evaluated by hematoxylin-eosin staining. aSignificantly different at p

    Techniques Used: Mouse Assay, Cell Differentiation, Immunohistochemistry, Staining

    25) Product Images from "Delayed and repeated intranasal delivery of bone marrow stromal cells increases regeneration and functional recovery after ischemic stroke in mice"

    Article Title: Delayed and repeated intranasal delivery of bone marrow stromal cells increases regeneration and functional recovery after ischemic stroke in mice

    Journal: BMC Neuroscience

    doi: 10.1186/s12868-018-0418-z

    Regenerative factors expressed in BMSCs. Immunocytochemistry was performed in cultured BSMCs for the expression of several regenerative factors. A – D Expressions of SDF-1α, VEGF, CXCR4, and FAK were detected in BMSCs. Scale bars represents 20 μm. E Reverse transcription PCR analysis confirms the expression of SDF-1α, VEGF, CXCR4, and FAK in four different batch of BMSCs
    Figure Legend Snippet: Regenerative factors expressed in BMSCs. Immunocytochemistry was performed in cultured BSMCs for the expression of several regenerative factors. A – D Expressions of SDF-1α, VEGF, CXCR4, and FAK were detected in BMSCs. Scale bars represents 20 μm. E Reverse transcription PCR analysis confirms the expression of SDF-1α, VEGF, CXCR4, and FAK in four different batch of BMSCs

    Techniques Used: Immunocytochemistry, Cell Culture, Expressing, Polymerase Chain Reaction

    26) Product Images from "Vascular Endothelial Growth Factor-dependent Spinogenesis Underlies Antidepressant-like Effects of Enriched Environment *"

    Article Title: Vascular Endothelial Growth Factor-dependent Spinogenesis Underlies Antidepressant-like Effects of Enriched Environment *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M112.392076

    Inhibition of miR-107 increases dendritic spine number through the activation of VEGF/Flk-1 signaling. A and B , representative images and summary graph showing the number of dendritic spines in hippocampal neuronal cultures from WT or Flk-1 +/− mice subjected to VEGF (100 ng/ml) treatment for 24 h or transfection with antagomiR-107. Con , control; Vec , vector. C and D , representative images and summary graph showing the number of dendritic spines in antagomiR-107-transfected neuronal cultures subjected to VEGF treatment or shRNA-HIF-1α co-transfection. E , levels of VEGF-A protein secretion in hippocampal neuronal cultures from WT or Flk-1 +/− mice in response to Vec or antagomiR-107 treatments. The total number of dendrites examined or experiments performed is indicated by n in parentheses . Data are presented as means ± S.E. *, p
    Figure Legend Snippet: Inhibition of miR-107 increases dendritic spine number through the activation of VEGF/Flk-1 signaling. A and B , representative images and summary graph showing the number of dendritic spines in hippocampal neuronal cultures from WT or Flk-1 +/− mice subjected to VEGF (100 ng/ml) treatment for 24 h or transfection with antagomiR-107. Con , control; Vec , vector. C and D , representative images and summary graph showing the number of dendritic spines in antagomiR-107-transfected neuronal cultures subjected to VEGF treatment or shRNA-HIF-1α co-transfection. E , levels of VEGF-A protein secretion in hippocampal neuronal cultures from WT or Flk-1 +/− mice in response to Vec or antagomiR-107 treatments. The total number of dendrites examined or experiments performed is indicated by n in parentheses . Data are presented as means ± S.E. *, p

    Techniques Used: Inhibition, Activation Assay, Mouse Assay, Transfection, Plasmid Preparation, shRNA, Cotransfection

    VEGF stimulates spinogenesis through the activation of Flk-1 receptors. A and C , representative images and summary graph showing the number of dendritic spines in shRNA-DsRed- or shRNA-Flk-1-transfected hippocampal neuronal cultures in response to VEGF (100 ng/ml) treatment for 24 h. B and D , representative images and summary graph showing the number of dendritic spines in vector ( Vec )- or DN-Flk-1-transfected hippocampal neuronal cultures in response to VEGF (100 ng/ml) treatment for 24 h. The total number of dendrites examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p
    Figure Legend Snippet: VEGF stimulates spinogenesis through the activation of Flk-1 receptors. A and C , representative images and summary graph showing the number of dendritic spines in shRNA-DsRed- or shRNA-Flk-1-transfected hippocampal neuronal cultures in response to VEGF (100 ng/ml) treatment for 24 h. B and D , representative images and summary graph showing the number of dendritic spines in vector ( Vec )- or DN-Flk-1-transfected hippocampal neuronal cultures in response to VEGF (100 ng/ml) treatment for 24 h. The total number of dendrites examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p

    Techniques Used: Activation Assay, shRNA, Transfection, Plasmid Preparation

    27) Product Images from "Matrix metalloproteinase 9 is associated with peritoneal membrane solute transport and induces angiogenesis through β-catenin signaling"

    Article Title: Matrix metalloproteinase 9 is associated with peritoneal membrane solute transport and induces angiogenesis through β-catenin signaling

    Journal: Nephrology Dialysis Transplantation

    doi: 10.1093/ndt/gfw076

    ( A – F ) Histology of the peritoneal membrane from C57Bl/6, MMP2 −/− and MMP9 −/− mice after adenovirus gene transfer of TGF-β1. C57Bl/6, MMP2 −/− and MMP9 −/− mice appear to have similar responses to TGF-β1. ( G ) Confirmation by western blot of MMP2 and MMP9 knock-out status. ( H ) Quantification of submesothelial thickness displays no significant difference between wild-type, MMP2 −/− and MMP9 −/− mice treated with TGF-β1. ( I ) Quantification of blood vessel density shows that TGF-β1 resulted in an increase in blood vessel density in wild-type and MMP2 −/− mice, whereas MMP9 −/− mice did not experience an increase in blood vessel density in response to AdTGFB1. ( J ) ELISA analysis of peritoneal effluent displays significantly increased levels of VEGF in C57Bl/6 mice and MMP2 −/− mice treated with TGF-β but not in MMP9 −/− mice.
    Figure Legend Snippet: ( A – F ) Histology of the peritoneal membrane from C57Bl/6, MMP2 −/− and MMP9 −/− mice after adenovirus gene transfer of TGF-β1. C57Bl/6, MMP2 −/− and MMP9 −/− mice appear to have similar responses to TGF-β1. ( G ) Confirmation by western blot of MMP2 and MMP9 knock-out status. ( H ) Quantification of submesothelial thickness displays no significant difference between wild-type, MMP2 −/− and MMP9 −/− mice treated with TGF-β1. ( I ) Quantification of blood vessel density shows that TGF-β1 resulted in an increase in blood vessel density in wild-type and MMP2 −/− mice, whereas MMP9 −/− mice did not experience an increase in blood vessel density in response to AdTGFB1. ( J ) ELISA analysis of peritoneal effluent displays significantly increased levels of VEGF in C57Bl/6 mice and MMP2 −/− mice treated with TGF-β but not in MMP9 −/− mice.

    Techniques Used: Mouse Assay, Western Blot, Knock-Out, Enzyme-linked Immunosorbent Assay

    Histology of the peritoneal membrane from C57Bl/6 mice 10 days after adenovirus gene transfer of control adenovirus (AdDL) or AdMMP9. ( A ) AdDL does not significantly alter the peritoneal membrane histology. ( B ) AdMMP9 led to submesothelial thickening and fibrosis (sections stained with Masson's trichrome, 200× magnification). ( C and D ) Factor VIII–stained sections of C57Bl/6 mouse peritoneum after adenovirus gene transfer of ( C ) AdDL or ( D ) AdMMP9 ( D ) (100× magnification). ( E and F ) Quantification of factor VIII–stained sections demonstrates an increase in submesothelial thickness after treatment with ( E ) AdMMP9 with ( F ) an increase in blood vessel density. ( G ) Increased angiogenesis was associated with a significant increase in VEGF measured in the peritoneal effluent. ( H ) Representative zymogram from peritoneal effluent. The first two lanes are positive controls. ( I ) Quantification shows increased MMP9 in mice receiving AdMMP9 along with ( J ) an increase in MMP2 expression.
    Figure Legend Snippet: Histology of the peritoneal membrane from C57Bl/6 mice 10 days after adenovirus gene transfer of control adenovirus (AdDL) or AdMMP9. ( A ) AdDL does not significantly alter the peritoneal membrane histology. ( B ) AdMMP9 led to submesothelial thickening and fibrosis (sections stained with Masson's trichrome, 200× magnification). ( C and D ) Factor VIII–stained sections of C57Bl/6 mouse peritoneum after adenovirus gene transfer of ( C ) AdDL or ( D ) AdMMP9 ( D ) (100× magnification). ( E and F ) Quantification of factor VIII–stained sections demonstrates an increase in submesothelial thickness after treatment with ( E ) AdMMP9 with ( F ) an increase in blood vessel density. ( G ) Increased angiogenesis was associated with a significant increase in VEGF measured in the peritoneal effluent. ( H ) Representative zymogram from peritoneal effluent. The first two lanes are positive controls. ( I ) Quantification shows increased MMP9 in mice receiving AdMMP9 along with ( J ) an increase in MMP2 expression.

    Techniques Used: Mouse Assay, Staining, Expressing

    Factor VIII–stained sections of C57Bl/6 mouse peritoneum after adenoviral gene transfer. ( A ) AdDL is a control virus and demonstrates the normal mouse peritoneum. ( B ) MMP9 induces an increase in blood vessel density and submesothelial thickness in the peritoneum. ( C ) ICG-001 inhibits the angiogenic response to MMP9. ICG-001 does not induce a significant reduction in submesothelial thickness. ( D ) Quantification of submesothelial thickness. ( E ) Quantification of angiogenesis. ( F and G ) VEGF expression in peritoneal tissue is reduced by ICG-001 treatment. ( F ) Representative blot quantified in ( G ).
    Figure Legend Snippet: Factor VIII–stained sections of C57Bl/6 mouse peritoneum after adenoviral gene transfer. ( A ) AdDL is a control virus and demonstrates the normal mouse peritoneum. ( B ) MMP9 induces an increase in blood vessel density and submesothelial thickness in the peritoneum. ( C ) ICG-001 inhibits the angiogenic response to MMP9. ICG-001 does not induce a significant reduction in submesothelial thickness. ( D ) Quantification of submesothelial thickness. ( E ) Quantification of angiogenesis. ( F and G ) VEGF expression in peritoneal tissue is reduced by ICG-001 treatment. ( F ) Representative blot quantified in ( G ).

    Techniques Used: Staining, Expressing

    28) Product Images from "The anti-tumor properties of two tumstatin peptide fragments in human gastric carcinoma"

    Article Title: The anti-tumor properties of two tumstatin peptide fragments in human gastric carcinoma

    Journal: Acta Pharmacologica Sinica

    doi: 10.1038/aps.2009.111

    Immunohistochemical expression of Fas; FasL; caspase3; Bcl-2; Bax; VEGF and bFGF in orthotopic gastric carcinoma samples or orthotopic gastric carcinoma treated with peptide 19 and peptide 21. Plasma or membrane staining was frequently observed in tumour cells treated with peptide 19 (A, B, C, D, and E; Fas; FasL; caspase 3; Bcl-2 and Bax, respectively A×400, B×400, C×200, D×400, and E×200). Absent expression of bFGF (F×200) or VEGF (G×200) was observed in tumour cells treated with peptide 21. Expression of bFGF (H×200) and VEGF (I×400) were high in orthotopic gastric carcinoma samples without treatment.
    Figure Legend Snippet: Immunohistochemical expression of Fas; FasL; caspase3; Bcl-2; Bax; VEGF and bFGF in orthotopic gastric carcinoma samples or orthotopic gastric carcinoma treated with peptide 19 and peptide 21. Plasma or membrane staining was frequently observed in tumour cells treated with peptide 19 (A, B, C, D, and E; Fas; FasL; caspase 3; Bcl-2 and Bax, respectively A×400, B×400, C×200, D×400, and E×200). Absent expression of bFGF (F×200) or VEGF (G×200) was observed in tumour cells treated with peptide 21. Expression of bFGF (H×200) and VEGF (I×400) were high in orthotopic gastric carcinoma samples without treatment.

    Techniques Used: Immunohistochemistry, Expressing, Staining

    29) Product Images from "High Glucose Increases Lysyl Oxidase Expression and Activity in Retinal Endothelial Cells: Mechanism for Compromised Extracellular Matrix Barrier Function"

    Article Title: High Glucose Increases Lysyl Oxidase Expression and Activity in Retinal Endothelial Cells: Mechanism for Compromised Extracellular Matrix Barrier Function

    Journal: Diabetes

    doi: 10.2337/db10-0365

    Western blot analysis of LOX protein levels in RRECs grown in normal (N) medium and stimulated with VEGF for 24 or 48 h. Graph shows LOX protein level was not significantly changed in cells stimulated with 25 ng/ml of VEGF for 24 h, although after 48 h of VEGF stimulation, LOX expression was significantly increased compared with cells grown in normal medium. Data are presented as mean ± SD (* P
    Figure Legend Snippet: Western blot analysis of LOX protein levels in RRECs grown in normal (N) medium and stimulated with VEGF for 24 or 48 h. Graph shows LOX protein level was not significantly changed in cells stimulated with 25 ng/ml of VEGF for 24 h, although after 48 h of VEGF stimulation, LOX expression was significantly increased compared with cells grown in normal medium. Data are presented as mean ± SD (* P

    Techniques Used: Western Blot, Expressing

    30) Product Images from "Prevention of Vasa Vasorum Neovascularization Attenuates Early Neointima Formation in Experimental Hypercholesterolemia"

    Article Title: Prevention of Vasa Vasorum Neovascularization Attenuates Early Neointima Formation in Experimental Hypercholesterolemia

    Journal: Basic research in cardiology

    doi: 10.1007/s00395-009-0036-0

    Co-localization of each NFkB, VEGF and TNF-α with vWF. Except for VEGF-vWF in the N+Th group there was no further co-localization found in the N and N+Th groups. Both HC and HC+Th groups showed co-localization of all four markers.
    Figure Legend Snippet: Co-localization of each NFkB, VEGF and TNF-α with vWF. Except for VEGF-vWF in the N+Th group there was no further co-localization found in the N and N+Th groups. Both HC and HC+Th groups showed co-localization of all four markers.

    Techniques Used:

    Co-localization of NFkB p65, VEGF and TNF-α with vWF. A, D, G are NFkB p65, VEGF, and TNF-α, respectively. B, E, and H are vWF. C, F, I are overlays of A and B, D and E, and G and H. Scale: 50μm.
    Figure Legend Snippet: Co-localization of NFkB p65, VEGF and TNF-α with vWF. A, D, G are NFkB p65, VEGF, and TNF-α, respectively. B, E, and H are vWF. C, F, I are overlays of A and B, D and E, and G and H. Scale: 50μm.

    Techniques Used:

    31) Product Images from "Enhancing the anti-angiogenic action of histone deacetylase inhibitors"

    Article Title: Enhancing the anti-angiogenic action of histone deacetylase inhibitors

    Journal: Molecular Cancer

    doi: 10.1186/1476-4598-6-68

    HDACI and IFNα co-operatively inhibit endothelial cell functions, and pro-angiogenic gene expression in cancer cells under hypoxic conditions in vitro . A. Human umbilical vein endothelial cells (HUVECs) were treated with control (Cont), 0.1 μM TSA and/or 500 IU/ml IFNα for 18 hours. Cell viability was evaluated with the Alamar blue assay. B. HUVECs were plated in BD Biosciences Fluroblok chambers and treated with control, 0.1 μM TSA and/or 500 IU/ml IFNα for 22 hours. Cells were stained with Cell Tracker Green CMFDA, migrated through chamber filters toward the chemo-attractant VEGF, and then quantified and expressed as optical density (OD) absorbance units. C. HUVECs were plated into BD BioCoat growth factor-reduced matrigel invasion chambers and treated with control, 0.1 μM TSA and/or 500 IU/ml IFNα for 18 hours. Cells which invaded through the Matrigel were fixed, stained with a Diff Quick staining kit, photographed and then quantified. D. HUVECs were plated onto growth factor-reduced Matrigel in 24 well plates and treated with control, 0.1 μM TSA and/or 500 IU/ml IFNα for 18 hours. Vascular sprouting was quantified by counting the numbers of complete branches per branching point. E. Neuroblastoma BE(2)-C cells were treated with control, 0.02 μM TSA and/or 500 IU/ml IFNα for 72 hours under hypoxic (1% O 2 ) conditions. RNA was extracted and subjected to independent semi-competitive RT-PCR analyses using trans-intron PCR primers, together with primers for the house-keeping gene β-2 microglobulin (β2M). Representative gels for each gene at the 72 hour time point were shown, and fold induction of a target gene by treatment was calculated by ascribing the ratio between the level of expression of a target gene and that of β2M as 1.0 for control treated samples. * p
    Figure Legend Snippet: HDACI and IFNα co-operatively inhibit endothelial cell functions, and pro-angiogenic gene expression in cancer cells under hypoxic conditions in vitro . A. Human umbilical vein endothelial cells (HUVECs) were treated with control (Cont), 0.1 μM TSA and/or 500 IU/ml IFNα for 18 hours. Cell viability was evaluated with the Alamar blue assay. B. HUVECs were plated in BD Biosciences Fluroblok chambers and treated with control, 0.1 μM TSA and/or 500 IU/ml IFNα for 22 hours. Cells were stained with Cell Tracker Green CMFDA, migrated through chamber filters toward the chemo-attractant VEGF, and then quantified and expressed as optical density (OD) absorbance units. C. HUVECs were plated into BD BioCoat growth factor-reduced matrigel invasion chambers and treated with control, 0.1 μM TSA and/or 500 IU/ml IFNα for 18 hours. Cells which invaded through the Matrigel were fixed, stained with a Diff Quick staining kit, photographed and then quantified. D. HUVECs were plated onto growth factor-reduced Matrigel in 24 well plates and treated with control, 0.1 μM TSA and/or 500 IU/ml IFNα for 18 hours. Vascular sprouting was quantified by counting the numbers of complete branches per branching point. E. Neuroblastoma BE(2)-C cells were treated with control, 0.02 μM TSA and/or 500 IU/ml IFNα for 72 hours under hypoxic (1% O 2 ) conditions. RNA was extracted and subjected to independent semi-competitive RT-PCR analyses using trans-intron PCR primers, together with primers for the house-keeping gene β-2 microglobulin (β2M). Representative gels for each gene at the 72 hour time point were shown, and fold induction of a target gene by treatment was calculated by ascribing the ratio between the level of expression of a target gene and that of β2M as 1.0 for control treated samples. * p

    Techniques Used: Expressing, In Vitro, Alamar Blue Assay, Staining, Diff-Quik, Reverse Transcription Polymerase Chain Reaction, Polymerase Chain Reaction

    32) Product Images from "An angiogenic role for the human peptide antibiotic LL-37/hCAP-18"

    Article Title: An angiogenic role for the human peptide antibiotic LL-37/hCAP-18

    Journal: Journal of Clinical Investigation

    doi: 10.1172/JCI200317545

    Effects of LL-37 on endothelial cells in vitro. ( a ) In vitro proliferation assays. Different concentrations of LL-37 and controls were added to cultivated HUVECs. Numbers at the left of the graph indicate the numbers of cells per microliter of volume after 72 hours. VEGF was used as positive control. Additionally, we tested sLL-37, HNP-1, -2, and -3, hBD-3, and the propeptides hCAP-18. In vitro proliferation was not inhibited by human serum. Application of the FPRL1 agonist peptide WKYMVm (W peptide) results in increased growth of cell numbers. Addition of antiserum to FPRL1 blunted increased cellular proliferation induced by LL-37. * P
    Figure Legend Snippet: Effects of LL-37 on endothelial cells in vitro. ( a ) In vitro proliferation assays. Different concentrations of LL-37 and controls were added to cultivated HUVECs. Numbers at the left of the graph indicate the numbers of cells per microliter of volume after 72 hours. VEGF was used as positive control. Additionally, we tested sLL-37, HNP-1, -2, and -3, hBD-3, and the propeptides hCAP-18. In vitro proliferation was not inhibited by human serum. Application of the FPRL1 agonist peptide WKYMVm (W peptide) results in increased growth of cell numbers. Addition of antiserum to FPRL1 blunted increased cellular proliferation induced by LL-37. * P

    Techniques Used: In Vitro, Positive Control

    33) Product Images from "Rapid production of human liver scaffolds for functional tissue engineering by high shear stress oscillation-decellularization"

    Article Title: Rapid production of human liver scaffolds for functional tissue engineering by high shear stress oscillation-decellularization

    Journal: Scientific Reports

    doi: 10.1038/s41598-017-05134-1

    Neo-angiogenesis and re-endothelisation of ALTCs. CAM assay of ( A ), decellularized liver cube, ( B ), sponge soaked in PBS, and ( C ), sponge loaded with VEGF. ( D ) Quantification of observed vessels at 0 and 7 days, showing a significant difference between the ALTCs after 7 days when compared to the negative control (PBS). Recellularization of ALTCs with HUVECs after 7 days, characterized by positive staining with ( E–G ), H E, ( H–J) , CD31 and ( K–M) , FVIII, confirming the migration and attachment of the endothelial cells to the lumen of the vessels and their functionality. Data are expressed as mean ± sem. *p
    Figure Legend Snippet: Neo-angiogenesis and re-endothelisation of ALTCs. CAM assay of ( A ), decellularized liver cube, ( B ), sponge soaked in PBS, and ( C ), sponge loaded with VEGF. ( D ) Quantification of observed vessels at 0 and 7 days, showing a significant difference between the ALTCs after 7 days when compared to the negative control (PBS). Recellularization of ALTCs with HUVECs after 7 days, characterized by positive staining with ( E–G ), H E, ( H–J) , CD31 and ( K–M) , FVIII, confirming the migration and attachment of the endothelial cells to the lumen of the vessels and their functionality. Data are expressed as mean ± sem. *p

    Techniques Used: Chick Chorioallantoic Membrane Assay, Negative Control, Staining, Migration

    34) Product Images from "Long non-coding RNA HEIH contributes to diabetic retinopathy by regulating miR-939/VEGF axis"

    Article Title: Long non-coding RNA HEIH contributes to diabetic retinopathy by regulating miR-939/VEGF axis

    Journal: International Journal of Clinical and Experimental Pathology

    doi:

    miR-939 regulated HG-induced APRE-19 cell injury through targeting VEGF. A: The mRNA and protein expression of VEGF after transfection with pEX-VEGF, sh-VEGF, and their controls. B: Cell viability in the treated groups. C: Cell apoptosis in the treated groups and the expression levels of apoptosis-related proteins. D: Cytochrome C release form mitochondria to cytoplasm in the treated groups. E: Caspase-3 activity in the treated groups. F: The regulatory effects of HEIH/miR-939/VEGF axis on protein expression of PI3K/AKT signaling pathway-related proteins in the HG-treated APRE-19 cells. All experiments were repeated three times and the data are presented as the mean ± SD. *P
    Figure Legend Snippet: miR-939 regulated HG-induced APRE-19 cell injury through targeting VEGF. A: The mRNA and protein expression of VEGF after transfection with pEX-VEGF, sh-VEGF, and their controls. B: Cell viability in the treated groups. C: Cell apoptosis in the treated groups and the expression levels of apoptosis-related proteins. D: Cytochrome C release form mitochondria to cytoplasm in the treated groups. E: Caspase-3 activity in the treated groups. F: The regulatory effects of HEIH/miR-939/VEGF axis on protein expression of PI3K/AKT signaling pathway-related proteins in the HG-treated APRE-19 cells. All experiments were repeated three times and the data are presented as the mean ± SD. *P

    Techniques Used: Expressing, Transfection, Activity Assay

    35) Product Images from "Targeting the angiotensin II type 2 receptor (AT2R) in colorectal liver metastases"

    Article Title: Targeting the angiotensin II type 2 receptor (AT2R) in colorectal liver metastases

    Journal: Cancer Cell International

    doi: 10.1186/1475-2867-10-19

    CD34 staining of neoangiogenic vessels in treated and untreated animals inoculated with MoCR cells in the liver (A) . Examples of high, medium, and low VEGF-expressing tumours (MoCR metastases growing in the liver) are shown for both control and treated animals (from left to right, respectively). Tumour (T) and infiltrating (I) cells are indicated. ELISA was used to examine VEGF secreted into medium conditioned by MoCR cells treated with CGP42112A at either 1 μM or 0.1 μM in a background of 0.1% FBS/RPMI. Significant P values are shown with an * and solid line, while those of interest with P values between 0.1 and 0.05 are indicated with a dotted line and no *. Data are presented as mean ± S.E.M.
    Figure Legend Snippet: CD34 staining of neoangiogenic vessels in treated and untreated animals inoculated with MoCR cells in the liver (A) . Examples of high, medium, and low VEGF-expressing tumours (MoCR metastases growing in the liver) are shown for both control and treated animals (from left to right, respectively). Tumour (T) and infiltrating (I) cells are indicated. ELISA was used to examine VEGF secreted into medium conditioned by MoCR cells treated with CGP42112A at either 1 μM or 0.1 μM in a background of 0.1% FBS/RPMI. Significant P values are shown with an * and solid line, while those of interest with P values between 0.1 and 0.05 are indicated with a dotted line and no *. Data are presented as mean ± S.E.M.

    Techniques Used: Staining, Expressing, Enzyme-linked Immunosorbent Assay

    36) Product Images from "Hypoxia Response Element-Regulated MMP-9 Promotes Neurological Recovery via Glial Scar Degradation and Angiogenesis in Delayed Stroke"

    Article Title: Hypoxia Response Element-Regulated MMP-9 Promotes Neurological Recovery via Glial Scar Degradation and Angiogenesis in Delayed Stroke

    Journal: Molecular Therapy

    doi: 10.1016/j.ymthe.2017.03.020

    MMP-9 Promoted Neurogenesis and Synaptogenesis, Depending on Angiogenesis in the Peri-infarct Area after tMCAO (A) Representative images of BrdU/NeuN double staining for neo-neurons (upper panel) and Lectin/GFAP double staining for vessels (lower panel) in the peri-infarct area 3 weeks after tMCAO. (B and C) Quantifications of BrdU + /NeuN + cell (B) and Lectin + vessel (C) number per field in NS-, GFP-, MMP-9-, SB-3CT-, and SU5416-treated mice at 3 weeks after tMCAO. Scale bar, 30 μm in BrdU and NeuN images and 50 μm in Lectin and GFAP images (N = 6 mice per group). (D and E) Western blot for PSD 95, Synaptophysin, VEGF, and VEGFR2 (D) and their quantifications (E) in NS-, GFP-, MMP-9-, SB-3CT-, and SU5416-treated mice at 3 weeks after tMCAO (N = 3 mice per group). (F) Quantitative of RT-PCR analysis of the expression of PSD 95 and synaptophysin in NS-, GFP-, MMP-9-, SB-3CT-, and SU-treated mice. Values were normalized to GAPDH (N = 3 mice per group). Data are mean ± SD. *p
    Figure Legend Snippet: MMP-9 Promoted Neurogenesis and Synaptogenesis, Depending on Angiogenesis in the Peri-infarct Area after tMCAO (A) Representative images of BrdU/NeuN double staining for neo-neurons (upper panel) and Lectin/GFAP double staining for vessels (lower panel) in the peri-infarct area 3 weeks after tMCAO. (B and C) Quantifications of BrdU + /NeuN + cell (B) and Lectin + vessel (C) number per field in NS-, GFP-, MMP-9-, SB-3CT-, and SU5416-treated mice at 3 weeks after tMCAO. Scale bar, 30 μm in BrdU and NeuN images and 50 μm in Lectin and GFAP images (N = 6 mice per group). (D and E) Western blot for PSD 95, Synaptophysin, VEGF, and VEGFR2 (D) and their quantifications (E) in NS-, GFP-, MMP-9-, SB-3CT-, and SU5416-treated mice at 3 weeks after tMCAO (N = 3 mice per group). (F) Quantitative of RT-PCR analysis of the expression of PSD 95 and synaptophysin in NS-, GFP-, MMP-9-, SB-3CT-, and SU-treated mice. Values were normalized to GAPDH (N = 3 mice per group). Data are mean ± SD. *p

    Techniques Used: Double Staining, Mouse Assay, Western Blot, Quantitative RT-PCR, Expressing

    37) Product Images from "SARI inhibits angiogenesis and tumour growth of human colon cancer through directly targeting ceruloplasmin"

    Article Title: SARI inhibits angiogenesis and tumour growth of human colon cancer through directly targeting ceruloplasmin

    Journal: Nature Communications

    doi: 10.1038/ncomms11996

    Reduction of VEGF by SARI. ( a ) Human angiogenesis array analysis of the conditional medium from SW480-controland SW480-SARI cells. ( b ) Summary of the relative signal intensity of indicated cytokines. ( c ) VEGF exacted from SW480 and HCT116 cells was quantified by ELISA ( n =3; ** P
    Figure Legend Snippet: Reduction of VEGF by SARI. ( a ) Human angiogenesis array analysis of the conditional medium from SW480-controland SW480-SARI cells. ( b ) Summary of the relative signal intensity of indicated cytokines. ( c ) VEGF exacted from SW480 and HCT116 cells was quantified by ELISA ( n =3; ** P

    Techniques Used: Enzyme-linked Immunosorbent Assay

    SARI inhibits angiogenesis through inhibiting Cp expression and the activity of the HIF-1α/VEGF axis. ( a ) Immunoblots of SARI and HIF-1α expression in SW480 and HCT116 cells after stable expression of SARI. HCT116-control and HCT116-SARI cells were incubated under 1% O 2 for 48 h or treated with DMOG for 24 h. β-Actin was used as a loading control. ( b ) Immunoblots of Cp, HIF-1α and VEGF expression in control and SARI cells with or without PX-478 (45 μM) or Tm (4.0 μM) treatment under normoxia and hypoxia. GAPDH was used as the loading control. ( c ) Immunoblots of Cp, HIF-1α and VEGF expression in control and SARI cells after transfection with or without p-Cp plasmid under normoxia and hypoxia. GAPDH was used as the loading control. ( d ) Expression of VEGF exacted by SW480-control and SW480-SARI cells with or without Tm (4.0 μM) and PX-478 (45 μM) treatment, after transfection with or without Cp expression plasmid ( n =3; ** P
    Figure Legend Snippet: SARI inhibits angiogenesis through inhibiting Cp expression and the activity of the HIF-1α/VEGF axis. ( a ) Immunoblots of SARI and HIF-1α expression in SW480 and HCT116 cells after stable expression of SARI. HCT116-control and HCT116-SARI cells were incubated under 1% O 2 for 48 h or treated with DMOG for 24 h. β-Actin was used as a loading control. ( b ) Immunoblots of Cp, HIF-1α and VEGF expression in control and SARI cells with or without PX-478 (45 μM) or Tm (4.0 μM) treatment under normoxia and hypoxia. GAPDH was used as the loading control. ( c ) Immunoblots of Cp, HIF-1α and VEGF expression in control and SARI cells after transfection with or without p-Cp plasmid under normoxia and hypoxia. GAPDH was used as the loading control. ( d ) Expression of VEGF exacted by SW480-control and SW480-SARI cells with or without Tm (4.0 μM) and PX-478 (45 μM) treatment, after transfection with or without Cp expression plasmid ( n =3; ** P

    Techniques Used: Expressing, Activity Assay, Western Blot, Incubation, Transfection, Plasmid Preparation

    SARI inhibits VEGF expression by directly binding to Cp. ( a ) Co-immunoprecipitation products after adding anti-SARI antibody were separated by SDS–PAGE, and the differential band was analysed by MS. ( b ) Co-immunoprecipitation analysis of SW480-control and SW480-SARI cell lysates using anti-SARI and anti-Cp antibody. ( c ) Staining for Cp (green) and SARI (red) in SW480-control and SW480-SARI cells; DAPI staining for the nucleus. Scale bar, 50 μm. ( d ) Immunoblots of SARI and Cp expression in SW480 and HCT116-blank, control and SARI cells. GAPDH was used as a loading control. ( e ) Western blotting detection of Cp expression of collected nuclear and cytoplasmic proteins. Histone H3 was used as the nucleus loading control and β-actin as the cytoplasm loading control. ( f ) Immunoblots of Cp and VEGF expression in SW480-control and SW480-SARI cells with or without MG132 treatment. GAPDH was used as the loading control. ( g ) ELISA detection of VEGF expression in SW480-control and SW480-SARI cells with or without MG132 treatment. ( n =4; ** P
    Figure Legend Snippet: SARI inhibits VEGF expression by directly binding to Cp. ( a ) Co-immunoprecipitation products after adding anti-SARI antibody were separated by SDS–PAGE, and the differential band was analysed by MS. ( b ) Co-immunoprecipitation analysis of SW480-control and SW480-SARI cell lysates using anti-SARI and anti-Cp antibody. ( c ) Staining for Cp (green) and SARI (red) in SW480-control and SW480-SARI cells; DAPI staining for the nucleus. Scale bar, 50 μm. ( d ) Immunoblots of SARI and Cp expression in SW480 and HCT116-blank, control and SARI cells. GAPDH was used as a loading control. ( e ) Western blotting detection of Cp expression of collected nuclear and cytoplasmic proteins. Histone H3 was used as the nucleus loading control and β-actin as the cytoplasm loading control. ( f ) Immunoblots of Cp and VEGF expression in SW480-control and SW480-SARI cells with or without MG132 treatment. GAPDH was used as the loading control. ( g ) ELISA detection of VEGF expression in SW480-control and SW480-SARI cells with or without MG132 treatment. ( n =4; ** P

    Techniques Used: Expressing, Binding Assay, Immunoprecipitation, SDS Page, Mass Spectrometry, Staining, Western Blot, Enzyme-linked Immunosorbent Assay

    SARI inhibits expression of downstream targets in vivo . ( a ) Staining for VEGF (red) revealed less VEGF-positive cells in SARI than in controlSW480Matrigel plugs, Scale bar, 50 μm; VEGF-positive (%; VEGF positive per total cells; n =5; ** P
    Figure Legend Snippet: SARI inhibits expression of downstream targets in vivo . ( a ) Staining for VEGF (red) revealed less VEGF-positive cells in SARI than in controlSW480Matrigel plugs, Scale bar, 50 μm; VEGF-positive (%; VEGF positive per total cells; n =5; ** P

    Techniques Used: Expressing, In Vivo, Staining

    38) Product Images from "Endothelial p53 Deletion Improves Angiogenesis and Prevents Cardiac Fibrosis and Heart Failure Induced by Pressure Overload in Mice"

    Article Title: Endothelial p53 Deletion Improves Angiogenesis and Prevents Cardiac Fibrosis and Heart Failure Induced by Pressure Overload in Mice

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    doi: 10.1161/JAHA.115.001770

    Effect of endothelial p53 deletion on Hif1α and Vegf levels. A through F, Western blot analysis of cardiac Hif1α and Vegf protein levels in End.p53‐WT and End.p53‐KO mice at different time points after transverse aortic constriction (TAC) or sham operation (S). Representative membranes are shown in A (8 and 20 weeks after TAC) and D (7 days after TAC). * P
    Figure Legend Snippet: Effect of endothelial p53 deletion on Hif1α and Vegf levels. A through F, Western blot analysis of cardiac Hif1α and Vegf protein levels in End.p53‐WT and End.p53‐KO mice at different time points after transverse aortic constriction (TAC) or sham operation (S). Representative membranes are shown in A (8 and 20 weeks after TAC) and D (7 days after TAC). * P

    Techniques Used: Western Blot, Mouse Assay

    39) Product Images from "Triple-marker cardiac MRI detects sequential tissue changes of healing myocardium after a hydrogel-based therapy"

    Article Title: Triple-marker cardiac MRI detects sequential tissue changes of healing myocardium after a hydrogel-based therapy

    Journal: Scientific Reports

    doi: 10.1038/s41598-019-55864-7

    UPy GF -hydrogel characterization and in vivo setup. ( a) In vitro release of IGF1/VEGF embedded in the UPy GF -hydrogel by daily collection of medium at 37 °C over one week (mean ± s.e.m, n = 4 measurements). ( b ) Localization of intramyocardial delivery of UPy GF -hydrogel 2 min before reperfusion in a mouse model of myocardial ischemia reperfusion (I/R). pH-switchable UPy GF -hydrogel loaded with insulin-like growth factor 1 (IGF1) and vascular endothelial growth factor (VEGF) in a solution state during basic conditions. After local injection, the UPy GF -hydrogel slowly released insulin-like growth factor 1 (IGF1) and vascular endothelial growth factor (VEGF). ( c ) Proof-of-concept ex vivo T 2 * MRI to verify intramyocardial UPy GF -hydrogel injections (arrows) labeled with ultrasmall superparamagnetic iron oxide at an infarcted heart 30 min after I/R. ( d ) In vivo experimental set-up of serial cardiac magnetic resonance imaging (MRI) and histology of hearts before and after I/R. The illustration of the heart (1b) and the mouse (1d) were modified from Servier Medical Art ( http://smart.servier.com/ ), licensed under a Creative Common Attribution 3.0 Generic License.
    Figure Legend Snippet: UPy GF -hydrogel characterization and in vivo setup. ( a) In vitro release of IGF1/VEGF embedded in the UPy GF -hydrogel by daily collection of medium at 37 °C over one week (mean ± s.e.m, n = 4 measurements). ( b ) Localization of intramyocardial delivery of UPy GF -hydrogel 2 min before reperfusion in a mouse model of myocardial ischemia reperfusion (I/R). pH-switchable UPy GF -hydrogel loaded with insulin-like growth factor 1 (IGF1) and vascular endothelial growth factor (VEGF) in a solution state during basic conditions. After local injection, the UPy GF -hydrogel slowly released insulin-like growth factor 1 (IGF1) and vascular endothelial growth factor (VEGF). ( c ) Proof-of-concept ex vivo T 2 * MRI to verify intramyocardial UPy GF -hydrogel injections (arrows) labeled with ultrasmall superparamagnetic iron oxide at an infarcted heart 30 min after I/R. ( d ) In vivo experimental set-up of serial cardiac magnetic resonance imaging (MRI) and histology of hearts before and after I/R. The illustration of the heart (1b) and the mouse (1d) were modified from Servier Medical Art ( http://smart.servier.com/ ), licensed under a Creative Common Attribution 3.0 Generic License.

    Techniques Used: In Vivo, In Vitro, Injection, Ex Vivo, Magnetic Resonance Imaging, Labeling, Modification

    40) Product Images from "Exosomes from adipose-derived stem cells overexpressing Nrf2 accelerate cutaneous wound healing by promoting vascularization in a diabetic foot ulcer rat model"

    Article Title: Exosomes from adipose-derived stem cells overexpressing Nrf2 accelerate cutaneous wound healing by promoting vascularization in a diabetic foot ulcer rat model

    Journal: Experimental & Molecular Medicine

    doi: 10.1038/s12276-018-0058-5

    Exosomes (Exos) derived from adipose-derived stem cells (ADSCs) overexpressing Nrf2 prevent high glucose (HG)-induced senescence by inhibiting ROS and inflammatory cytokine expression. a , b The level of Nrf2 in exosomes secreted from ADSCs with or without Nrf2 overexpression. c Proliferation of EPC cells was analyzed by the MTT assay with different concentrations of Exos from ADSCs (ADSC-Exo) or Nrf2 overexpression ADSCs (Nrf2-ADSC-Exo) after exposure to high glucose (HG, 30 mM) for 48 h. d Tube formation capability detected in endothelial progenitor cells (EPCs) stimulated with 50 μg/ml ADSC-Exo or Nrf2-ADSC-Exo for 12 h under HG (30 mM) condition. e – j Western blot analysis and protein expression levels of SMP30, VEGF, VEGFR, and NOX1/4 after stimulation with ADSC-Exo or Nrf2-ADSC-Exo for 12 h under HG (30 mM) condition. GAPDH served as an internal control. The relative protein levels were analyzed, and data are presented as the mean ± SD ( n = 3). *** P
    Figure Legend Snippet: Exosomes (Exos) derived from adipose-derived stem cells (ADSCs) overexpressing Nrf2 prevent high glucose (HG)-induced senescence by inhibiting ROS and inflammatory cytokine expression. a , b The level of Nrf2 in exosomes secreted from ADSCs with or without Nrf2 overexpression. c Proliferation of EPC cells was analyzed by the MTT assay with different concentrations of Exos from ADSCs (ADSC-Exo) or Nrf2 overexpression ADSCs (Nrf2-ADSC-Exo) after exposure to high glucose (HG, 30 mM) for 48 h. d Tube formation capability detected in endothelial progenitor cells (EPCs) stimulated with 50 μg/ml ADSC-Exo or Nrf2-ADSC-Exo for 12 h under HG (30 mM) condition. e – j Western blot analysis and protein expression levels of SMP30, VEGF, VEGFR, and NOX1/4 after stimulation with ADSC-Exo or Nrf2-ADSC-Exo for 12 h under HG (30 mM) condition. GAPDH served as an internal control. The relative protein levels were analyzed, and data are presented as the mean ± SD ( n = 3). *** P

    Techniques Used: Derivative Assay, Expressing, Over Expression, MTT Assay, Western Blot

    Related Articles

    Generated:

    Article Title: Genome-wide association identifies a deletion in the 3' untranslated region of Striatin in a canine model of arrhythmogenic right ventricular cardiomyopathy
    Article Snippet: .. Membranes were blocked with 5% milk and Striatin epitopes were probed by both a mouse monoclonal antibody generated against a WD repeat region (amino acid 450–600) of Striatin (1:100) (BD Transduction Laboratories, Franklin Lakes, NJ, USA) and a rabbit polyclonal antibody against a synthetic Striatin peptide which does not cross react with SG2NA (1:300) (Millipore). .. Blots were stripped and also probed with actin monoclonal antibody (1:100) (BD Transduction Laboratories) as a loading control.

    Article Title: Evidence for coordinated interaction of cyclin D3 with p21 and cdk6 in directing the development of uterine stromal cell decidualization and polyploidy during implantation
    Article Snippet: .. Rabbit polyclonal antibody to p21 (Cat# PC55), generated against a recombinant protein consisting amino acids 15–61 of mouse p21, was purchased from Oncogene Research Products (Cambridge, MA). .. A monoclonal antibody for p27, obtained from mouse ascites by epitope-affinity chromatography using full-length human recombinant p27 protein, was obtained from Zymed Laboratories Inc. (San Francisco, CA).

    Recombinant:

    Article Title: Evidence for coordinated interaction of cyclin D3 with p21 and cdk6 in directing the development of uterine stromal cell decidualization and polyploidy during implantation
    Article Snippet: .. Rabbit polyclonal antibody to p21 (Cat# PC55), generated against a recombinant protein consisting amino acids 15–61 of mouse p21, was purchased from Oncogene Research Products (Cambridge, MA). .. A monoclonal antibody for p27, obtained from mouse ascites by epitope-affinity chromatography using full-length human recombinant p27 protein, was obtained from Zymed Laboratories Inc. (San Francisco, CA).

    Affinity Purification:

    Article Title: Dopamine D1-like Receptors Regulate Constitutive, μ-Opioid Receptor-Mediated Repression of Use-Dependent Synaptic Plasticity in Dorsal Horn Neurons: More Harm than Good?
    Article Snippet: .. We used an affinity-purified goat polyclonal antibody against D1R (E-16; sc-31479 from Santa Cruz Biotechnology) at 1:1000 and a rabbit polyclonal antibody to met-enkephalin (Millipore) 1:1000 as primary antibodies. .. The goat polyclonal antibody to D1R was tested for band specificity and no cross-reactivity with D5R (the other member of the D1R-like subfamily) in samples from HEK293T cells transfected with either D1R-myc or D5R-myc (cf. below).

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    • mouse monoclonal anti vegf antibody  (Millipore)
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    Millipore mouse monoclonal anti vegf antibody
    Kinesin-1B associates with vesicular transport of <t>VEGF.</t> (A) Biochemical association of kinesin-1B with VEGF vesicles. An antibody specific for kinesin-1B was used to pull-down associated membrane components from isolated vesicles, including VEGF vesicles (indicated in Figure 1F ). Anti-GFP antibody was used as a control. The bead-bound (bound) and unbound fractions (unbound) were analyzed by <t>immunoblotting</t> with antibodies specific for the indicated proteins. (B,C) Simultaneous transfection of VEGF-eGFP plasmids and kinesin-1B -DsRed plasmids at 5 DIV (days in vitro ), and distributions of VEGF-eGFP and kinesin-1B -DsRed were detected by immunostaining with axonal specific marker SMI 312 at 48 h after transfection. The representative images show VEGF and kinesin-1B co-localization in SMI 312 positive axon, as indicated by arrows in (C) . Panel (C) is magnified images of box in (B) . Scale bars = 50 μm (B) ; 5 μm (C) . (D–G) Anterograde (D,E) and retrograde (F,G) co-transport of VEGF and kinesin-1B. The first frame (D,F) and kymograph (E,G) of VEGF (green in merged image) and kinesin-1B (magenta in merged image) are provided. Time (in seconds) and distance (in micrometers) are labeled on merged kymographs. Measured segments were masked by lines with different colors, green lines represented as VEGF vesicles, red lines represented as kinesin-B vesicles, yellow lines represented as merged vesicles. Scale bars = 7.5 μm (D,F) . (H) Accumulative data of average velocity of co-transported puntas from four or three independent experiments. (I) Quantification of the percentages of anterograde and retrograde co-transported punctas among total co-transported punctas in four independent experiments. (J,K) Histograms for segmental velocity of anterograde co-transported punctas (J) and retrograde co-transported punctas (K) . Ns means the number of segments. Antero and Retro represent anterograde and retrograde, respectively. Data represent mean ± S.E.M.
    Mouse Monoclonal Anti Vegf Antibody, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    vegf a  (Millipore)
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    Millipore vegf a
    Effects of ABL on <t>VEGF-induced</t> HUVEC migration and tube formation. A-B) ABL increases VEGF-induced ECs transwell migration. The data represent the number of migrated cells per microscopic field in VEGF-treated cells vs. control cells. C-D) ABL increases VEGF-induced EC transwell migration. Confluent HUVECs in a monolayer were pretreated with ABL or vehicle for 2 h and wounded with a cell scraper. After 48 h of incubation at 37°C, the number of cells that migrated across the wound edge was counted in each field. E-F) ABL increases VEGF-induced EC tube formation. The images were visualized using a phase contrast microscope (10× magnification). The total tubule length from 10 non-overlapping fields was measured by tracing the tube-like structure. The values represent the mean ± SEM from 3 independent experiments ( n = 3). Scale bar: 100 μm.
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    <t>VEGF</t> siRNA-generating pDNA down regulates VEGF <t>mRNA</t> levels in rat cervix . The VEGF gene silencing efficiency of the selected siRNA-generating pDNA was tested in vivo in the cervix of pregnant rat from GD17–20. VEGF siRNA-generating pDNA was found to down-regulate VEGF compared to control. n = 5, ( p
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    Kinesin-1B associates with vesicular transport of VEGF. (A) Biochemical association of kinesin-1B with VEGF vesicles. An antibody specific for kinesin-1B was used to pull-down associated membrane components from isolated vesicles, including VEGF vesicles (indicated in Figure 1F ). Anti-GFP antibody was used as a control. The bead-bound (bound) and unbound fractions (unbound) were analyzed by immunoblotting with antibodies specific for the indicated proteins. (B,C) Simultaneous transfection of VEGF-eGFP plasmids and kinesin-1B -DsRed plasmids at 5 DIV (days in vitro ), and distributions of VEGF-eGFP and kinesin-1B -DsRed were detected by immunostaining with axonal specific marker SMI 312 at 48 h after transfection. The representative images show VEGF and kinesin-1B co-localization in SMI 312 positive axon, as indicated by arrows in (C) . Panel (C) is magnified images of box in (B) . Scale bars = 50 μm (B) ; 5 μm (C) . (D–G) Anterograde (D,E) and retrograde (F,G) co-transport of VEGF and kinesin-1B. The first frame (D,F) and kymograph (E,G) of VEGF (green in merged image) and kinesin-1B (magenta in merged image) are provided. Time (in seconds) and distance (in micrometers) are labeled on merged kymographs. Measured segments were masked by lines with different colors, green lines represented as VEGF vesicles, red lines represented as kinesin-B vesicles, yellow lines represented as merged vesicles. Scale bars = 7.5 μm (D,F) . (H) Accumulative data of average velocity of co-transported puntas from four or three independent experiments. (I) Quantification of the percentages of anterograde and retrograde co-transported punctas among total co-transported punctas in four independent experiments. (J,K) Histograms for segmental velocity of anterograde co-transported punctas (J) and retrograde co-transported punctas (K) . Ns means the number of segments. Antero and Retro represent anterograde and retrograde, respectively. Data represent mean ± S.E.M.

    Journal: Frontiers in Molecular Neuroscience

    Article Title: VEGF Axonal Transport Dependent on Kinesin-1B and Microtubules Dynamics

    doi: 10.3389/fnmol.2017.00424

    Figure Lengend Snippet: Kinesin-1B associates with vesicular transport of VEGF. (A) Biochemical association of kinesin-1B with VEGF vesicles. An antibody specific for kinesin-1B was used to pull-down associated membrane components from isolated vesicles, including VEGF vesicles (indicated in Figure 1F ). Anti-GFP antibody was used as a control. The bead-bound (bound) and unbound fractions (unbound) were analyzed by immunoblotting with antibodies specific for the indicated proteins. (B,C) Simultaneous transfection of VEGF-eGFP plasmids and kinesin-1B -DsRed plasmids at 5 DIV (days in vitro ), and distributions of VEGF-eGFP and kinesin-1B -DsRed were detected by immunostaining with axonal specific marker SMI 312 at 48 h after transfection. The representative images show VEGF and kinesin-1B co-localization in SMI 312 positive axon, as indicated by arrows in (C) . Panel (C) is magnified images of box in (B) . Scale bars = 50 μm (B) ; 5 μm (C) . (D–G) Anterograde (D,E) and retrograde (F,G) co-transport of VEGF and kinesin-1B. The first frame (D,F) and kymograph (E,G) of VEGF (green in merged image) and kinesin-1B (magenta in merged image) are provided. Time (in seconds) and distance (in micrometers) are labeled on merged kymographs. Measured segments were masked by lines with different colors, green lines represented as VEGF vesicles, red lines represented as kinesin-B vesicles, yellow lines represented as merged vesicles. Scale bars = 7.5 μm (D,F) . (H) Accumulative data of average velocity of co-transported puntas from four or three independent experiments. (I) Quantification of the percentages of anterograde and retrograde co-transported punctas among total co-transported punctas in four independent experiments. (J,K) Histograms for segmental velocity of anterograde co-transported punctas (J) and retrograde co-transported punctas (K) . Ns means the number of segments. Antero and Retro represent anterograde and retrograde, respectively. Data represent mean ± S.E.M.

    Article Snippet: The pellets were eluted with beta-mercaptoethanol and used for further immunoblotting assay with rabbit anti-KIF5B antibody (1:1,000, Abcam) or mouse monoclonal anti-VEGF antibody (1:500, Millipore), respectively.

    Techniques: Isolation, Transfection, In Vitro, Immunostaining, Marker, Labeling

    Effects of ABL on VEGF-induced HUVEC migration and tube formation. A-B) ABL increases VEGF-induced ECs transwell migration. The data represent the number of migrated cells per microscopic field in VEGF-treated cells vs. control cells. C-D) ABL increases VEGF-induced EC transwell migration. Confluent HUVECs in a monolayer were pretreated with ABL or vehicle for 2 h and wounded with a cell scraper. After 48 h of incubation at 37°C, the number of cells that migrated across the wound edge was counted in each field. E-F) ABL increases VEGF-induced EC tube formation. The images were visualized using a phase contrast microscope (10× magnification). The total tubule length from 10 non-overlapping fields was measured by tracing the tube-like structure. The values represent the mean ± SEM from 3 independent experiments ( n = 3). Scale bar: 100 μm.

    Journal: PLoS ONE

    Article Title: Acetylbritannilactone Modulates Vascular Endothelial Growth Factor Signaling and Regulates Angiogenesis in Endothelial Cells

    doi: 10.1371/journal.pone.0148968

    Figure Lengend Snippet: Effects of ABL on VEGF-induced HUVEC migration and tube formation. A-B) ABL increases VEGF-induced ECs transwell migration. The data represent the number of migrated cells per microscopic field in VEGF-treated cells vs. control cells. C-D) ABL increases VEGF-induced EC transwell migration. Confluent HUVECs in a monolayer were pretreated with ABL or vehicle for 2 h and wounded with a cell scraper. After 48 h of incubation at 37°C, the number of cells that migrated across the wound edge was counted in each field. E-F) ABL increases VEGF-induced EC tube formation. The images were visualized using a phase contrast microscope (10× magnification). The total tubule length from 10 non-overlapping fields was measured by tracing the tube-like structure. The values represent the mean ± SEM from 3 independent experiments ( n = 3). Scale bar: 100 μm.

    Article Snippet: The next day, pretreated the cells with vehicle or different doses of ABL, followed by exposure of some of the wells (n = 16) to VEGF-A (50 ng/mL) for 48 h. Cell growth was assessed using an MTT assay (Millipore Corporation, Temecula, CA, USA) according to the manufacturer’s protocol.

    Techniques: Migration, Incubation, Microscopy

    Schematic representation of the ABL effect on VEGF signaling in ECs. ABL inhibits VEGFR-2 and VE-cadherin association, thus promoting VEGFR-2 internalization, following by VEGF-induced VEGFR-2 phosphorylation and downstream signaling.

    Journal: PLoS ONE

    Article Title: Acetylbritannilactone Modulates Vascular Endothelial Growth Factor Signaling and Regulates Angiogenesis in Endothelial Cells

    doi: 10.1371/journal.pone.0148968

    Figure Lengend Snippet: Schematic representation of the ABL effect on VEGF signaling in ECs. ABL inhibits VEGFR-2 and VE-cadherin association, thus promoting VEGFR-2 internalization, following by VEGF-induced VEGFR-2 phosphorylation and downstream signaling.

    Article Snippet: The next day, pretreated the cells with vehicle or different doses of ABL, followed by exposure of some of the wells (n = 16) to VEGF-A (50 ng/mL) for 48 h. Cell growth was assessed using an MTT assay (Millipore Corporation, Temecula, CA, USA) according to the manufacturer’s protocol.

    Techniques:

    ABL enhances VEGF signaling in endothelial cells. A) HUVECs were serum-starved overnight and pretreated with ABL or vehicle for 2 h, followed by exposure to VEGF-A (50 ng/mL) for various times as indicated. MAPK MAPK p44/42 Thr202/Tyr204 , p38 Thr180/Tyr182 , and Akt Ser473 phosphorylation in the cell lysates were measured via western blot analysis. B-D) The quantitative analysis represents the ratio of phosphorylated/total MAPK MAPK p44/42, MAPK p38, and Akt from 3 independent experiments. E) VEGFR-2 Tyr1175 phosphorylation in the cell lysates was measured via western blot analysis. F) Quantitative analysis of the ratio of phosphorylated/total VEGFR-2 from three independent experiments ( n = 3).

    Journal: PLoS ONE

    Article Title: Acetylbritannilactone Modulates Vascular Endothelial Growth Factor Signaling and Regulates Angiogenesis in Endothelial Cells

    doi: 10.1371/journal.pone.0148968

    Figure Lengend Snippet: ABL enhances VEGF signaling in endothelial cells. A) HUVECs were serum-starved overnight and pretreated with ABL or vehicle for 2 h, followed by exposure to VEGF-A (50 ng/mL) for various times as indicated. MAPK MAPK p44/42 Thr202/Tyr204 , p38 Thr180/Tyr182 , and Akt Ser473 phosphorylation in the cell lysates were measured via western blot analysis. B-D) The quantitative analysis represents the ratio of phosphorylated/total MAPK MAPK p44/42, MAPK p38, and Akt from 3 independent experiments. E) VEGFR-2 Tyr1175 phosphorylation in the cell lysates was measured via western blot analysis. F) Quantitative analysis of the ratio of phosphorylated/total VEGFR-2 from three independent experiments ( n = 3).

    Article Snippet: The next day, pretreated the cells with vehicle or different doses of ABL, followed by exposure of some of the wells (n = 16) to VEGF-A (50 ng/mL) for 48 h. Cell growth was assessed using an MTT assay (Millipore Corporation, Temecula, CA, USA) according to the manufacturer’s protocol.

    Techniques: Western Blot

    ABL increases VEGF-induced HUVEC growth and proliferation. A) VEGF-induced EC growth monitored by the MTT assay following treatment with different doses of ABL or vehicle. The data represent the percent increase after 48 h relative to non-stimulated cells from 3 independent experiments. B) VEGF-induced [ 3 H]-thymidine incorporation following different doses of ABL or vehicle. The data represent the percent increase after 48 h relative to the non-stimulated cells from 3 independent experiments ( n = 3). * P

    Journal: PLoS ONE

    Article Title: Acetylbritannilactone Modulates Vascular Endothelial Growth Factor Signaling and Regulates Angiogenesis in Endothelial Cells

    doi: 10.1371/journal.pone.0148968

    Figure Lengend Snippet: ABL increases VEGF-induced HUVEC growth and proliferation. A) VEGF-induced EC growth monitored by the MTT assay following treatment with different doses of ABL or vehicle. The data represent the percent increase after 48 h relative to non-stimulated cells from 3 independent experiments. B) VEGF-induced [ 3 H]-thymidine incorporation following different doses of ABL or vehicle. The data represent the percent increase after 48 h relative to the non-stimulated cells from 3 independent experiments ( n = 3). * P

    Article Snippet: The next day, pretreated the cells with vehicle or different doses of ABL, followed by exposure of some of the wells (n = 16) to VEGF-A (50 ng/mL) for 48 h. Cell growth was assessed using an MTT assay (Millipore Corporation, Temecula, CA, USA) according to the manufacturer’s protocol.

    Techniques: MTT Assay

    ABL enhances VEGFR-2 internalization in ECs. A) Colocalization of VEGFR-2 with endosome markers EEA1 in ECs. The ECs were pretreated with ABL for 2 h following fifteen minutes of VEGF stimulation, fixed, permeablized, and labeled with anti-VEGFR-2 (red) and anti-EEA1 (green) and processed for confocal microscopy. The endocytic trafficking of VEGFR2 without locating in endosome was observed in ECs (arrow). B) Colocalization of VEGFR-2 (red) and VE-cadherin (green) was observed in ECs (arrow). Nuclei were counterstained with DAPI (blue). Scale bar = 20 μm.

    Journal: PLoS ONE

    Article Title: Acetylbritannilactone Modulates Vascular Endothelial Growth Factor Signaling and Regulates Angiogenesis in Endothelial Cells

    doi: 10.1371/journal.pone.0148968

    Figure Lengend Snippet: ABL enhances VEGFR-2 internalization in ECs. A) Colocalization of VEGFR-2 with endosome markers EEA1 in ECs. The ECs were pretreated with ABL for 2 h following fifteen minutes of VEGF stimulation, fixed, permeablized, and labeled with anti-VEGFR-2 (red) and anti-EEA1 (green) and processed for confocal microscopy. The endocytic trafficking of VEGFR2 without locating in endosome was observed in ECs (arrow). B) Colocalization of VEGFR-2 (red) and VE-cadherin (green) was observed in ECs (arrow). Nuclei were counterstained with DAPI (blue). Scale bar = 20 μm.

    Article Snippet: The next day, pretreated the cells with vehicle or different doses of ABL, followed by exposure of some of the wells (n = 16) to VEGF-A (50 ng/mL) for 48 h. Cell growth was assessed using an MTT assay (Millipore Corporation, Temecula, CA, USA) according to the manufacturer’s protocol.

    Techniques: Labeling, Confocal Microscopy

    ABL enhances Matrigel angiogenesis in vivo . A) Examples of CD31 immunofluorescence staining of Matrigel plugs containing VEGF-A or control buffer. B) The quantification data represent the percent increase in CD31-positive area in comparison with the control sample ( n = 6). C) Quantitative analysis of GAPDH-normalized VE-cadherin ( Cdh5 ) mRNA expression in Matrigel plugs containing VEGF-A or control buffer that were implanted in mice ( n = 3). Scale bars: 100 μm.

    Journal: PLoS ONE

    Article Title: Acetylbritannilactone Modulates Vascular Endothelial Growth Factor Signaling and Regulates Angiogenesis in Endothelial Cells

    doi: 10.1371/journal.pone.0148968

    Figure Lengend Snippet: ABL enhances Matrigel angiogenesis in vivo . A) Examples of CD31 immunofluorescence staining of Matrigel plugs containing VEGF-A or control buffer. B) The quantification data represent the percent increase in CD31-positive area in comparison with the control sample ( n = 6). C) Quantitative analysis of GAPDH-normalized VE-cadherin ( Cdh5 ) mRNA expression in Matrigel plugs containing VEGF-A or control buffer that were implanted in mice ( n = 3). Scale bars: 100 μm.

    Article Snippet: The next day, pretreated the cells with vehicle or different doses of ABL, followed by exposure of some of the wells (n = 16) to VEGF-A (50 ng/mL) for 48 h. Cell growth was assessed using an MTT assay (Millipore Corporation, Temecula, CA, USA) according to the manufacturer’s protocol.

    Techniques: In Vivo, Immunofluorescence, Staining, Expressing, Mouse Assay

    Inhibition of VEGF-A-mediated PI3K/Akt pathway in HUVECs. The HUVECs were serum-starved for 24 h and stimulated in fresh medium with VEGF-A (25 ng/ml) and then treated with HY (0.062 μM) in combination with VEGF-A (25 ng/ml) for 24 h. The cells were exposed to a 585-nm LED light at a dose of 1.0 J/cm 2 and were incubation for 24 h. The cells were lysed and the proteins were harvested for western blot analysis of VEGF-A ( a ), p-Akt (Ser473) and Akt ( b ), and Bad ( c ). Densitometric measurements were analysed using AlphaEaseFC 4.0 software. The protein expression levels were normalized to those of the vehicle control (100%). Data are presented as means ± S.D. (n = 3); ** P

    Journal: Scientific Reports

    Article Title: Hypericin-photodynamic therapy induces human umbilical vein endothelial cell apoptosis

    doi: 10.1038/srep18398

    Figure Lengend Snippet: Inhibition of VEGF-A-mediated PI3K/Akt pathway in HUVECs. The HUVECs were serum-starved for 24 h and stimulated in fresh medium with VEGF-A (25 ng/ml) and then treated with HY (0.062 μM) in combination with VEGF-A (25 ng/ml) for 24 h. The cells were exposed to a 585-nm LED light at a dose of 1.0 J/cm 2 and were incubation for 24 h. The cells were lysed and the proteins were harvested for western blot analysis of VEGF-A ( a ), p-Akt (Ser473) and Akt ( b ), and Bad ( c ). Densitometric measurements were analysed using AlphaEaseFC 4.0 software. The protein expression levels were normalized to those of the vehicle control (100%). Data are presented as means ± S.D. (n = 3); ** P

    Article Snippet: The proteins were separated by 10% or 12% (for Bcl-2, Bax, cleaved caspase-9, procaspase-3, cleaved PARP, VEGF-A, phospho-Akt (Ser473, p-Akt), Akt, Bad and β-Actin) SDS-polyacrylamide gels and electrophoretically transferred onto PVDF membranes (Millipore, Massachusetts, USA).

    Techniques: Inhibition, Incubation, Western Blot, Software, Expressing

    VEGF siRNA-generating pDNA down regulates VEGF mRNA levels in rat cervix . The VEGF gene silencing efficiency of the selected siRNA-generating pDNA was tested in vivo in the cervix of pregnant rat from GD17–20. VEGF siRNA-generating pDNA was found to down-regulate VEGF compared to control. n = 5, ( p

    Journal: Reproductive Biology and Endocrinology : RB & E

    Article Title: Delineation of VEGF-regulated genes and functions in the cervix of pregnant rodents by DNA microarray analysis

    doi: 10.1186/1477-7827-6-64

    Figure Lengend Snippet: VEGF siRNA-generating pDNA down regulates VEGF mRNA levels in rat cervix . The VEGF gene silencing efficiency of the selected siRNA-generating pDNA was tested in vivo in the cervix of pregnant rat from GD17–20. VEGF siRNA-generating pDNA was found to down-regulate VEGF compared to control. n = 5, ( p

    Article Snippet: Cervices were harvested, processed and evaluated for changes in levels of VEGF mRNA and whole genome gene expression using DNA microarray data, as described below. b) Pregnant mice and ovariectomized non-pregnant rats and mice treated with either mouse recombinant VEGF protein (10 ng/mouse recombinant VEGF; Calbiochem, La Jolla, CA, once daily from GD13–17, intra-vaginally), VEGF receptor antagonist (as described earlier, but treated daily), or vehicle only, were utilized to confirm the DNA microarray data above using real-time PCR, and for morphological studies (SEM), described below.

    Techniques: In Vivo

    VEGF siRNA-generating pDNA down regulates VEGF mRNA levels in rat heart fibroblasts . The VEGF gene silencing efficiency by the three siRNA-generating pDNAs were tested in vitro using rat heart fibroblast primary cell transfection. VEGF siRNA-generating pDNA was found to down-regulate VEGF in cultured rat heart fibroblasts compared to control. The pDNA with the best silencing efficiency was selected and used in the rat cervix to test its efficiency to down-regulate local cervical VEGF in vivo (see Figure 2). n = 5, ( p

    Journal: Reproductive Biology and Endocrinology : RB & E

    Article Title: Delineation of VEGF-regulated genes and functions in the cervix of pregnant rodents by DNA microarray analysis

    doi: 10.1186/1477-7827-6-64

    Figure Lengend Snippet: VEGF siRNA-generating pDNA down regulates VEGF mRNA levels in rat heart fibroblasts . The VEGF gene silencing efficiency by the three siRNA-generating pDNAs were tested in vitro using rat heart fibroblast primary cell transfection. VEGF siRNA-generating pDNA was found to down-regulate VEGF in cultured rat heart fibroblasts compared to control. The pDNA with the best silencing efficiency was selected and used in the rat cervix to test its efficiency to down-regulate local cervical VEGF in vivo (see Figure 2). n = 5, ( p

    Article Snippet: Cervices were harvested, processed and evaluated for changes in levels of VEGF mRNA and whole genome gene expression using DNA microarray data, as described below. b) Pregnant mice and ovariectomized non-pregnant rats and mice treated with either mouse recombinant VEGF protein (10 ng/mouse recombinant VEGF; Calbiochem, La Jolla, CA, once daily from GD13–17, intra-vaginally), VEGF receptor antagonist (as described earlier, but treated daily), or vehicle only, were utilized to confirm the DNA microarray data above using real-time PCR, and for morphological studies (SEM), described below.

    Techniques: In Vitro, Transfection, Cell Culture, In Vivo