recombinant vegf  (R&D Systems)

 
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94
    Name:
    Recombinant Canine VEGF Protein
    Description:
    The Recombinant Canine VEGF Protein from R D Systems is derived from E coli The Recombinant Canine VEGF Protein has been validated for the following applications Bioactivity
    Catalog Number:
    1603-cv-010
    Price:
    329
    Category:
    Proteins and Enzymes
    Source:
    E. coli-derived Recombinant Canine VEGF Protein
    Applications:
    Bioactivity
    Purity:
    >95%, by SDS-PAGE under reducing conditions and visualized by silver stain
    Conjugate:
    Unconjugated
    Size:
    10 ug
    Buy from Supplier


    Structured Review

    R&D Systems recombinant vegf
    In vivo angiogenesis is augmented in SCD chimeric mice and inhibited by hydroxyurea. A <t>Matrigel</t> plug neovascularization assay was employed to compare neovascularization in SCD chimeric (SS) and C57BL/6 mice and observe the effects of hydroxyurea on in vivo vessel formation. The following were injected subcutaneously into C57BL/6 and SS mice; a mixture of Matrigel and heparin without vascular endothelial growth factor <t>(VEGF−,</t> negative control); Matrigel, heparin and VEGF (VEGF +, positive control) or Matrigel, heparin, VEGF and 100 μM hydroxy -urea (VEGF+HU). Matrigel plugs were left in place for 7 days. (A) Quantification of hemoglobin (Hb) in the homogenized Matrigel plugs using Drabkin solution, results are expressed as Hb content in the Matrigel plug (mg/g) (mean±SEM; C57BL/6, n=5; SS, n=4–6). (B) Representative photomicrographs of Matrigel plugs. Scale bars, 1 cm.* P
    The Recombinant Canine VEGF Protein from R D Systems is derived from E coli The Recombinant Canine VEGF Protein has been validated for the following applications Bioactivity
    https://www.bioz.com/result/recombinant vegf/product/R&D Systems
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant vegf - by Bioz Stars, 2021-03
    94/100 stars

    Images

    1) Product Images from "Key endothelial cell angiogenic mechanisms are stimulated by the circulating milieu in sickle cell disease and attenuated by hydroxyurea"

    Article Title: Key endothelial cell angiogenic mechanisms are stimulated by the circulating milieu in sickle cell disease and attenuated by hydroxyurea

    Journal: Haematologica

    doi: 10.3324/haematol.2014.119727

    In vivo angiogenesis is augmented in SCD chimeric mice and inhibited by hydroxyurea. A Matrigel plug neovascularization assay was employed to compare neovascularization in SCD chimeric (SS) and C57BL/6 mice and observe the effects of hydroxyurea on in vivo vessel formation. The following were injected subcutaneously into C57BL/6 and SS mice; a mixture of Matrigel and heparin without vascular endothelial growth factor (VEGF−, negative control); Matrigel, heparin and VEGF (VEGF +, positive control) or Matrigel, heparin, VEGF and 100 μM hydroxy -urea (VEGF+HU). Matrigel plugs were left in place for 7 days. (A) Quantification of hemoglobin (Hb) in the homogenized Matrigel plugs using Drabkin solution, results are expressed as Hb content in the Matrigel plug (mg/g) (mean±SEM; C57BL/6, n=5; SS, n=4–6). (B) Representative photomicrographs of Matrigel plugs. Scale bars, 1 cm.* P
    Figure Legend Snippet: In vivo angiogenesis is augmented in SCD chimeric mice and inhibited by hydroxyurea. A Matrigel plug neovascularization assay was employed to compare neovascularization in SCD chimeric (SS) and C57BL/6 mice and observe the effects of hydroxyurea on in vivo vessel formation. The following were injected subcutaneously into C57BL/6 and SS mice; a mixture of Matrigel and heparin without vascular endothelial growth factor (VEGF−, negative control); Matrigel, heparin and VEGF (VEGF +, positive control) or Matrigel, heparin, VEGF and 100 μM hydroxy -urea (VEGF+HU). Matrigel plugs were left in place for 7 days. (A) Quantification of hemoglobin (Hb) in the homogenized Matrigel plugs using Drabkin solution, results are expressed as Hb content in the Matrigel plug (mg/g) (mean±SEM; C57BL/6, n=5; SS, n=4–6). (B) Representative photomicrographs of Matrigel plugs. Scale bars, 1 cm.* P

    Techniques Used: In Vivo, Mouse Assay, Injection, Negative Control, Positive Control

    2) Product Images from "Novel role for SLPI in MOG-induced EAE revealed by spinal cord expression analysis"

    Article Title: Novel role for SLPI in MOG-induced EAE revealed by spinal cord expression analysis

    Journal: Journal of Neuroinflammation

    doi: 10.1186/1742-2094-5-20

    SLPI promotes proliferation of adult neural stem cells and induces cyclin D1 . A: Proliferation of rat neural stem cells after treatment with SLPI or VEGF, respectively. Cells were treated with indicated amounts of SLPI or VEGF for three days. Afterwards, they were pulsed with 10 μM BrdU. Proportion of BrdU-positive cells (+ std dev) was determined with the FITC BrdU Flow Kit. Presentation of a representative result of three experiments. *:p
    Figure Legend Snippet: SLPI promotes proliferation of adult neural stem cells and induces cyclin D1 . A: Proliferation of rat neural stem cells after treatment with SLPI or VEGF, respectively. Cells were treated with indicated amounts of SLPI or VEGF for three days. Afterwards, they were pulsed with 10 μM BrdU. Proportion of BrdU-positive cells (+ std dev) was determined with the FITC BrdU Flow Kit. Presentation of a representative result of three experiments. *:p

    Techniques Used: Flow Cytometry

    3) Product Images from "Retinal Inhibition of CCR3 Induces Retinal Cell Death in a Murine Model of Choroidal Neovascularization"

    Article Title: Retinal Inhibition of CCR3 Induces Retinal Cell Death in a Murine Model of Choroidal Neovascularization

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0157748

    Inhibition of CCR3 promotes cell death events in cultured human Műller cells. In cultured human MIO-M1 cells treated with PBS, CCL11, VEGF, or CCL11 and VEGF with pretreatment with CCR3i or control (DMSO), (A) western blots of CCR3 and VEGFR2. (B) TUNEL staining. (C) Quantification of TUNEL+ cells. (D) Western blots of cleaved caspase-3 and total caspase-3. (E) Western blots and quanfication of (F) BCL2 and (G) of AIF. (H) Western blots and (I) quanfication of BDNF (*p
    Figure Legend Snippet: Inhibition of CCR3 promotes cell death events in cultured human Műller cells. In cultured human MIO-M1 cells treated with PBS, CCL11, VEGF, or CCL11 and VEGF with pretreatment with CCR3i or control (DMSO), (A) western blots of CCR3 and VEGFR2. (B) TUNEL staining. (C) Quantification of TUNEL+ cells. (D) Western blots of cleaved caspase-3 and total caspase-3. (E) Western blots and quanfication of (F) BCL2 and (G) of AIF. (H) Western blots and (I) quanfication of BDNF (*p

    Techniques Used: Inhibition, Cell Culture, Western Blot, TUNEL Assay, Staining

    Inhibition of CCR3 in cultured human CECS reduces VEGF signaling without inducing cell death. In cultured human CECs treated with PBS or CCL11, VEGF or CCL11 and VEGF with or without pretreatment with CCR3i or control, (A) western blots of phosphorylated VEGFR2 (p-VEGFR2) and CCR3 and (B) quanfication of p-VEGFR2 (pretreatment with SU5416 was used as a control for inhibition of VEGFR2 activation) (**p
    Figure Legend Snippet: Inhibition of CCR3 in cultured human CECS reduces VEGF signaling without inducing cell death. In cultured human CECs treated with PBS or CCL11, VEGF or CCL11 and VEGF with or without pretreatment with CCR3i or control, (A) western blots of phosphorylated VEGFR2 (p-VEGFR2) and CCR3 and (B) quanfication of p-VEGFR2 (pretreatment with SU5416 was used as a control for inhibition of VEGFR2 activation) (**p

    Techniques Used: Inhibition, Cell Culture, Western Blot, Activation Assay

    4) Product Images from "Key endothelial cell angiogenic mechanisms are stimulated by the circulating milieu in sickle cell disease and attenuated by hydroxyurea"

    Article Title: Key endothelial cell angiogenic mechanisms are stimulated by the circulating milieu in sickle cell disease and attenuated by hydroxyurea

    Journal: Haematologica

    doi: 10.3324/haematol.2014.119727

    In vivo angiogenesis is augmented in SCD chimeric mice and inhibited by hydroxyurea. A Matrigel plug neovascularization assay was employed to compare neovascularization in SCD chimeric (SS) and C57BL/6 mice and observe the effects of hydroxyurea on in vivo vessel formation. The following were injected subcutaneously into C57BL/6 and SS mice; a mixture of Matrigel and heparin without vascular endothelial growth factor (VEGF−, negative control); Matrigel, heparin and VEGF (VEGF +, positive control) or Matrigel, heparin, VEGF and 100 μM hydroxy -urea (VEGF+HU). Matrigel plugs were left in place for 7 days. (A) Quantification of hemoglobin (Hb) in the homogenized Matrigel plugs using Drabkin solution, results are expressed as Hb content in the Matrigel plug (mg/g) (mean±SEM; C57BL/6, n=5; SS, n=4–6). (B) Representative photomicrographs of Matrigel plugs. Scale bars, 1 cm.* P
    Figure Legend Snippet: In vivo angiogenesis is augmented in SCD chimeric mice and inhibited by hydroxyurea. A Matrigel plug neovascularization assay was employed to compare neovascularization in SCD chimeric (SS) and C57BL/6 mice and observe the effects of hydroxyurea on in vivo vessel formation. The following were injected subcutaneously into C57BL/6 and SS mice; a mixture of Matrigel and heparin without vascular endothelial growth factor (VEGF−, negative control); Matrigel, heparin and VEGF (VEGF +, positive control) or Matrigel, heparin, VEGF and 100 μM hydroxy -urea (VEGF+HU). Matrigel plugs were left in place for 7 days. (A) Quantification of hemoglobin (Hb) in the homogenized Matrigel plugs using Drabkin solution, results are expressed as Hb content in the Matrigel plug (mg/g) (mean±SEM; C57BL/6, n=5; SS, n=4–6). (B) Representative photomicrographs of Matrigel plugs. Scale bars, 1 cm.* P

    Techniques Used: In Vivo, Mouse Assay, Injection, Negative Control, Positive Control

    5) Product Images from "Experimental and theoretical investigation of the precise transduction mechanism in giant magnetoresistive biosensors"

    Article Title: Experimental and theoretical investigation of the precise transduction mechanism in giant magnetoresistive biosensors

    Journal: Scientific Reports

    doi: 10.1038/srep18692

    VEGF and GCSF duplex assay. Anti-VEGF and anti-GCSF antibodies were immobilized on different sensors with quadruplicates. The sample containing VEGF at 500 pg/ml and GCSF at 500 pg/ml was measured. The nanoparticles were added to the chip at 2 min. The extra distance between the nanoparticles and the surface still produced the same positive signals with respect to the baseline signal (before adding the nanoparticles). BSA signals were the same as the baseline after adding the nanoparticles. The error bars are the standard deviations of 4 identical sensor signals.
    Figure Legend Snippet: VEGF and GCSF duplex assay. Anti-VEGF and anti-GCSF antibodies were immobilized on different sensors with quadruplicates. The sample containing VEGF at 500 pg/ml and GCSF at 500 pg/ml was measured. The nanoparticles were added to the chip at 2 min. The extra distance between the nanoparticles and the surface still produced the same positive signals with respect to the baseline signal (before adding the nanoparticles). BSA signals were the same as the baseline after adding the nanoparticles. The error bars are the standard deviations of 4 identical sensor signals.

    Techniques Used: Chromatin Immunoprecipitation, Produced

    6) Product Images from "Heparanase-enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis"

    Article Title: Heparanase-enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis

    Journal: Blood

    doi: 10.1182/blood-2009-07-234757

    Shed syndecan-1 and VEGF act together to stimulate ERK activation and endothelial invasion . (A) Syndecan-1 enhances VEGF-mediated invasion of endothelial cells. An endothelial invasion assay was performed with conditioned medium from HPSE-high cells that
    Figure Legend Snippet: Shed syndecan-1 and VEGF act together to stimulate ERK activation and endothelial invasion . (A) Syndecan-1 enhances VEGF-mediated invasion of endothelial cells. An endothelial invasion assay was performed with conditioned medium from HPSE-high cells that

    Techniques Used: Activated Clotting Time Assay, Activation Assay, Invasion Assay

    Medium conditioned by heparanase high myeloma cells enhances endothelial invasion via activity of VEGF . (A) Endothelial cells were seeded on the top well of an invasion chamber coated with Matrigel and conditioned medium from either HPSE-low or HPSE-high
    Figure Legend Snippet: Medium conditioned by heparanase high myeloma cells enhances endothelial invasion via activity of VEGF . (A) Endothelial cells were seeded on the top well of an invasion chamber coated with Matrigel and conditioned medium from either HPSE-low or HPSE-high

    Techniques Used: Activity Assay

    7) Product Images from "Netrin-4 inhibits angiogenesis via binding to neogenin and recruitment of Unc5B"

    Article Title: Netrin-4 inhibits angiogenesis via binding to neogenin and recruitment of Unc5B

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.0804008105

    N4 inhibits EC tube formation and migration induced by VEGF. ( A ) HUAEC were transfected with control siRNA or N4 siRNA before being incubated on top of Matrigel. Silencing the N4 gene in HUAEC increased both the branching and their ability to form tubular structures on Matrigel compared with nontransfected cells (NT) or with cells transfected with the control siRNA. RT-PCR analysis indicates that the N4 gene has been selectively silenced in N4 siRNA-treated HUAEC. ( B ) N4 does not affect the basal migration of growth-arrested HUAEC (C) but inhibits the migration induced by VEGF (V) as well as N1 (N1). ( C ) N1 and N4 inhibit the VEGF-induced FAK phosphorylation in HUAEC ( Upper ). ( Lower ) The total FAK immunoprecipitated. The ratio of phosphorylated FAK to total FAK is normalized to unstimulated HUAEC. **, P
    Figure Legend Snippet: N4 inhibits EC tube formation and migration induced by VEGF. ( A ) HUAEC were transfected with control siRNA or N4 siRNA before being incubated on top of Matrigel. Silencing the N4 gene in HUAEC increased both the branching and their ability to form tubular structures on Matrigel compared with nontransfected cells (NT) or with cells transfected with the control siRNA. RT-PCR analysis indicates that the N4 gene has been selectively silenced in N4 siRNA-treated HUAEC. ( B ) N4 does not affect the basal migration of growth-arrested HUAEC (C) but inhibits the migration induced by VEGF (V) as well as N1 (N1). ( C ) N1 and N4 inhibit the VEGF-induced FAK phosphorylation in HUAEC ( Upper ). ( Lower ) The total FAK immunoprecipitated. The ratio of phosphorylated FAK to total FAK is normalized to unstimulated HUAEC. **, P

    Techniques Used: Migration, Transfection, Incubation, Reverse Transcription Polymerase Chain Reaction, Immunoprecipitation

    ) or from retinal pigment epithelium (RPE) that have been exposed to VEGF (V) or not (0). Blots were probed for thrombospondin-1 (TSP-1), NPC-2, and N4. Band intensity ratios were normalized to 1 for non-VEGF-exposed cells.
    Figure Legend Snippet: ) or from retinal pigment epithelium (RPE) that have been exposed to VEGF (V) or not (0). Blots were probed for thrombospondin-1 (TSP-1), NPC-2, and N4. Band intensity ratios were normalized to 1 for non-VEGF-exposed cells.

    Techniques Used:

    Neogenin and Unc5B are required for N1- and N4-induced inhibition of HUAEC migration. ( A ) Anti-neogenin (red) antibody staining shows that NE is localized in filipodia of HUAEC. Upon incubation with N4, NE staining is relocalized in the perinuclear area. Nuclei are labeled in blue with DAPI. (Scale bars: 10 μm.) ( B ) Silencing either Unc5B or NE is sufficient to abrogate the chemotactic effect of N1 or N4. ( C ) The inhibition of N4 binding to NE abolishes its function whereas the inhibition of its binding to Unc5B or Unc5C has no effect. ( D ) Neogenin is equally detected in N4-unstimulated (0) and Netrin-4-stimulated HUAEC (0N4) or in VEGF-stimulated (V) or FGF-2-stimulated (F) HUAEC, whereas N4 increases the interaction between UNC5B and neogenin in VEGF-stimulated (VN4) or FGF-2-stimulated (FN4) HUAEC. Detection of neogenin in CHO-transfected cells served as a control (far right lane, NEO).
    Figure Legend Snippet: Neogenin and Unc5B are required for N1- and N4-induced inhibition of HUAEC migration. ( A ) Anti-neogenin (red) antibody staining shows that NE is localized in filipodia of HUAEC. Upon incubation with N4, NE staining is relocalized in the perinuclear area. Nuclei are labeled in blue with DAPI. (Scale bars: 10 μm.) ( B ) Silencing either Unc5B or NE is sufficient to abrogate the chemotactic effect of N1 or N4. ( C ) The inhibition of N4 binding to NE abolishes its function whereas the inhibition of its binding to Unc5B or Unc5C has no effect. ( D ) Neogenin is equally detected in N4-unstimulated (0) and Netrin-4-stimulated HUAEC (0N4) or in VEGF-stimulated (V) or FGF-2-stimulated (F) HUAEC, whereas N4 increases the interaction between UNC5B and neogenin in VEGF-stimulated (VN4) or FGF-2-stimulated (FN4) HUAEC. Detection of neogenin in CHO-transfected cells served as a control (far right lane, NEO).

    Techniques Used: Inhibition, Migration, Staining, Incubation, Labeling, Binding Assay, Transfection

    N4 is a neogenin ligand. ( A ) HUAEC and HUVEC express Unc5B (UB), Unc5C (UC), and neogenin (NE). The results are expressed relative to their abundance in human fetal brain and normalized to the β-actin mRNA content. ( B ) Immunoprecipitation of N1 and N4 by chimera of human Fc IgG fused to neogenin (NE), Unc5B (UB), or Unc5C (UC). VEGFR2 (VR2) is used as a negative control. ( C ) VEGF-driven HUAEC migration is inhibited by N4 and N1. The activity of N4 is almost totally abolished by addition of the chimera NE but not by chimera UB or UC. In contrast, N1 activity is inhibited by the three chimeras.
    Figure Legend Snippet: N4 is a neogenin ligand. ( A ) HUAEC and HUVEC express Unc5B (UB), Unc5C (UC), and neogenin (NE). The results are expressed relative to their abundance in human fetal brain and normalized to the β-actin mRNA content. ( B ) Immunoprecipitation of N1 and N4 by chimera of human Fc IgG fused to neogenin (NE), Unc5B (UB), or Unc5C (UC). VEGFR2 (VR2) is used as a negative control. ( C ) VEGF-driven HUAEC migration is inhibited by N4 and N1. The activity of N4 is almost totally abolished by addition of the chimera NE but not by chimera UB or UC. In contrast, N1 activity is inhibited by the three chimeras.

    Techniques Used: Immunoprecipitation, Negative Control, Migration, Activity Assay

    8) Product Images from "Experimental orthotopic transplantation of a tissue-engineered oesophagus in rats"

    Article Title: Experimental orthotopic transplantation of a tissue-engineered oesophagus in rats

    Journal: Nature Communications

    doi: 10.1038/ncomms4562

    Protein content and functional assays. ( a – d ) Expression of collagen I and IV in native ( a , c ) and decellularized ( b , d ) oesophagus (scale bar—Col I—50 μm, Col IV—20 μm, mu indicating muscular layer, l—lumen). An intact basement membrane is indicated by collagen IV expression ( c , d , red arrows). ( e – j ) Expression of elastin, fibronectin and laminin in native ( e , g , i , mu indicating muscular layer, sm submucosa) and decellularized ( f , h , j ) oesophagus (scale bar—25 μm). ( k , l ) Expression of VEGF factor in native ( k ) and decellularized ( l ) oesophagus (l—lumen, sm—submucosa, mu—muscular layer). VEGF and laminin-stained tubular structures, suggesting intact vasculature, are found in native and decellularized tissue ( i – l , inserts, scale bar—10 μm). ( m ) Protein quantification of extracellular matrix proteins ( n =3 biological replicates). ( n – q ) Angiogenesis assay implanted with gelfoam (control, asterisk in n ) and with fragments of decellularized oesophagus (asterisk in o ). The oesophagus induced new vessels, proving the scaffolds’ positive influence of vessel organization. SEM micrographs of vessel and the scaffold sample ( p , * ) and newly built vessel ( p , ↓) (scale bar—100 μm), higher magnification on one of the vessels( q ; scale bar—25 μm). ( r ) Quantification of blood vessels converging to the samples, indicating the strong angiogenic induction by the scaffold, at the levels of the positive control ( n =3). ( s ) The scaffold was inflated and deflated over 10,000 times, a stable plateau phase ( s ) proves the scaffold’s integrity in the last cycle, as there is no leakage from the scaffold ( n =3, one representative graph shown). ( t ) Axial strength was evaluated using burst pressure measurements, without any difference between native, decellularized or reseeded groups ( n =5). ( u , v ) Tensile test showed that strength lost during decellularization was regained after reseeding: force at break ( u ) and strain at break ( v ) ( n =5). ( w ) Distensibility assay showed that the lost distensibility after decellularization (black series) was regained after reseeding (green series) ( n =5), highly resembling the native organ (red series). * P
    Figure Legend Snippet: Protein content and functional assays. ( a – d ) Expression of collagen I and IV in native ( a , c ) and decellularized ( b , d ) oesophagus (scale bar—Col I—50 μm, Col IV—20 μm, mu indicating muscular layer, l—lumen). An intact basement membrane is indicated by collagen IV expression ( c , d , red arrows). ( e – j ) Expression of elastin, fibronectin and laminin in native ( e , g , i , mu indicating muscular layer, sm submucosa) and decellularized ( f , h , j ) oesophagus (scale bar—25 μm). ( k , l ) Expression of VEGF factor in native ( k ) and decellularized ( l ) oesophagus (l—lumen, sm—submucosa, mu—muscular layer). VEGF and laminin-stained tubular structures, suggesting intact vasculature, are found in native and decellularized tissue ( i – l , inserts, scale bar—10 μm). ( m ) Protein quantification of extracellular matrix proteins ( n =3 biological replicates). ( n – q ) Angiogenesis assay implanted with gelfoam (control, asterisk in n ) and with fragments of decellularized oesophagus (asterisk in o ). The oesophagus induced new vessels, proving the scaffolds’ positive influence of vessel organization. SEM micrographs of vessel and the scaffold sample ( p , * ) and newly built vessel ( p , ↓) (scale bar—100 μm), higher magnification on one of the vessels( q ; scale bar—25 μm). ( r ) Quantification of blood vessels converging to the samples, indicating the strong angiogenic induction by the scaffold, at the levels of the positive control ( n =3). ( s ) The scaffold was inflated and deflated over 10,000 times, a stable plateau phase ( s ) proves the scaffold’s integrity in the last cycle, as there is no leakage from the scaffold ( n =3, one representative graph shown). ( t ) Axial strength was evaluated using burst pressure measurements, without any difference between native, decellularized or reseeded groups ( n =5). ( u , v ) Tensile test showed that strength lost during decellularization was regained after reseeding: force at break ( u ) and strain at break ( v ) ( n =5). ( w ) Distensibility assay showed that the lost distensibility after decellularization (black series) was regained after reseeding (green series) ( n =5), highly resembling the native organ (red series). * P

    Techniques Used: Functional Assay, Expressing, Staining, Angiogenesis Assay, Positive Control

    9) Product Images from "Heparanase-enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis"

    Article Title: Heparanase-enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis

    Journal: Blood

    doi: 10.1182/blood-2009-07-234757

    Shed syndecan-1 and VEGF act together to stimulate ERK activation and endothelial invasion . (A) Syndecan-1 enhances VEGF-mediated invasion of endothelial cells. An endothelial invasion assay was performed with conditioned medium from HPSE-high cells that
    Figure Legend Snippet: Shed syndecan-1 and VEGF act together to stimulate ERK activation and endothelial invasion . (A) Syndecan-1 enhances VEGF-mediated invasion of endothelial cells. An endothelial invasion assay was performed with conditioned medium from HPSE-high cells that

    Techniques Used: Activated Clotting Time Assay, Activation Assay, Invasion Assay

    Medium conditioned by heparanase high myeloma cells enhances endothelial invasion via activity of VEGF . (A) Endothelial cells were seeded on the top well of an invasion chamber coated with Matrigel and conditioned medium from either HPSE-low or HPSE-high
    Figure Legend Snippet: Medium conditioned by heparanase high myeloma cells enhances endothelial invasion via activity of VEGF . (A) Endothelial cells were seeded on the top well of an invasion chamber coated with Matrigel and conditioned medium from either HPSE-low or HPSE-high

    Techniques Used: Activity Assay

    10) Product Images from "Differential effects of a soluble or immobilized VEGFR-binding peptide"

    Article Title: Differential effects of a soluble or immobilized VEGFR-binding peptide

    Journal: Integrative biology : quantitative biosciences from nano to macro

    doi: 10.1039/c2ib20055d

    HUVEC response to soluble morphogens. HUVECs starved overnight in 2% FBS were seeded on arrays presenting varied densities of GRGDSP in the presence of 2% FBS alone or with the addition of 10 ng/mL VR-BP (4.8 nM) or 10 ng/mL VEGF (0.26 nM). (Error bars indicate standard error of the mean and asterisk indicate significance compared to FBS alone, p
    Figure Legend Snippet: HUVEC response to soluble morphogens. HUVECs starved overnight in 2% FBS were seeded on arrays presenting varied densities of GRGDSP in the presence of 2% FBS alone or with the addition of 10 ng/mL VR-BP (4.8 nM) or 10 ng/mL VEGF (0.26 nM). (Error bars indicate standard error of the mean and asterisk indicate significance compared to FBS alone, p

    Techniques Used:

    11) Product Images from "Increased supply from blood vessels promotes the activation of dormant primordial follicles in mouse ovaries"

    Article Title: Increased supply from blood vessels promotes the activation of dormant primordial follicles in mouse ovaries

    Journal: The Journal of Reproduction and Development

    doi: 10.1262/jrd.2019-091

    Expression of KIT ligand (KITL) in 10-week-old ICR mouse ovaries in which a biodegradable gel containing vascular endothelial growth factor (VEGF) was transplanted and in cultured P0 mouse ovaries. (A) A primordial follicle that expressed KITL (KITL-positive primordial follicles) in a 10-week-old ICR mouse ovary. (B) Primordial follicles that did not express KITL in a 10-week-old ICR mouse ovary. (C) Ratio of KITL-positive primordial follicles in the ovaries in which a biodegradable gel containing 10 μg/ml recombinant VEGF was transplanted. (D) Ratio of KITL-positive primordial follicles in the cultured P0 mouse ovaries. Arrows indicate primordial follicles. Mean ± SD (n = 3 for 10 μg/ml recombinant VEGF, n = 5 for control; n = 3 for 10% fetal bovine serum (FBS), n = 4 for 5% FBS and n = 7 for 0% FBS). Scale bar: 50 μm. * P
    Figure Legend Snippet: Expression of KIT ligand (KITL) in 10-week-old ICR mouse ovaries in which a biodegradable gel containing vascular endothelial growth factor (VEGF) was transplanted and in cultured P0 mouse ovaries. (A) A primordial follicle that expressed KITL (KITL-positive primordial follicles) in a 10-week-old ICR mouse ovary. (B) Primordial follicles that did not express KITL in a 10-week-old ICR mouse ovary. (C) Ratio of KITL-positive primordial follicles in the ovaries in which a biodegradable gel containing 10 μg/ml recombinant VEGF was transplanted. (D) Ratio of KITL-positive primordial follicles in the cultured P0 mouse ovaries. Arrows indicate primordial follicles. Mean ± SD (n = 3 for 10 μg/ml recombinant VEGF, n = 5 for control; n = 3 for 10% fetal bovine serum (FBS), n = 4 for 5% FBS and n = 7 for 0% FBS). Scale bar: 50 μm. * P

    Techniques Used: Expressing, Cell Culture, Recombinant

    Effect of recombinant vascular endothelial growth factor (VEGF) on the activation of primordial follicles in cultured P0 Oog1pro3.9/R26-H2B-mCherry mouse ovaries. Mean ± SD (n = 3 for 200 ng/ml, n = 4 for 50 ng /ml, n = 5 for 100 ng /ml, and n = 12 for control.
    Figure Legend Snippet: Effect of recombinant vascular endothelial growth factor (VEGF) on the activation of primordial follicles in cultured P0 Oog1pro3.9/R26-H2B-mCherry mouse ovaries. Mean ± SD (n = 3 for 200 ng/ml, n = 4 for 50 ng /ml, n = 5 for 100 ng /ml, and n = 12 for control.

    Techniques Used: Recombinant, Activation Assay, Cell Culture

    12) Product Images from "Heparanase-enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis"

    Article Title: Heparanase-enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis

    Journal: Blood

    doi: 10.1182/blood-2009-07-234757

    Shed syndecan-1 and VEGF act together to stimulate ERK activation and endothelial invasion . (A) Syndecan-1 enhances VEGF-mediated invasion of endothelial cells. An endothelial invasion assay was performed with conditioned medium from HPSE-high cells that
    Figure Legend Snippet: Shed syndecan-1 and VEGF act together to stimulate ERK activation and endothelial invasion . (A) Syndecan-1 enhances VEGF-mediated invasion of endothelial cells. An endothelial invasion assay was performed with conditioned medium from HPSE-high cells that

    Techniques Used: Activated Clotting Time Assay, Activation Assay, Invasion Assay

    Medium conditioned by heparanase high myeloma cells enhances endothelial invasion via activity of VEGF . (A) Endothelial cells were seeded on the top well of an invasion chamber coated with Matrigel and conditioned medium from either HPSE-low or HPSE-high
    Figure Legend Snippet: Medium conditioned by heparanase high myeloma cells enhances endothelial invasion via activity of VEGF . (A) Endothelial cells were seeded on the top well of an invasion chamber coated with Matrigel and conditioned medium from either HPSE-low or HPSE-high

    Techniques Used: Activity Assay

    13) Product Images from "Heparanase-enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis"

    Article Title: Heparanase-enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis

    Journal: Blood

    doi: 10.1182/blood-2009-07-234757

    Shed syndecan-1 and VEGF act together to stimulate ERK activation and endothelial invasion . (A) Syndecan-1 enhances VEGF-mediated invasion of endothelial cells. An endothelial invasion assay was performed with conditioned medium from HPSE-high cells that
    Figure Legend Snippet: Shed syndecan-1 and VEGF act together to stimulate ERK activation and endothelial invasion . (A) Syndecan-1 enhances VEGF-mediated invasion of endothelial cells. An endothelial invasion assay was performed with conditioned medium from HPSE-high cells that

    Techniques Used: Activated Clotting Time Assay, Activation Assay, Invasion Assay

    14) Product Images from "Increased supply from blood vessels promotes the activation of dormant primordial follicles in mouse ovaries"

    Article Title: Increased supply from blood vessels promotes the activation of dormant primordial follicles in mouse ovaries

    Journal: The Journal of Reproduction and Development

    doi: 10.1262/jrd.2019-091

    Expression of KIT ligand (KITL) in 10-week-old ICR mouse ovaries in which a biodegradable gel containing vascular endothelial growth factor (VEGF) was transplanted and in cultured P0 mouse ovaries. (A) A primordial follicle that expressed KITL (KITL-positive primordial follicles) in a 10-week-old ICR mouse ovary. (B) Primordial follicles that did not express KITL in a 10-week-old ICR mouse ovary. (C) Ratio of KITL-positive primordial follicles in the ovaries in which a biodegradable gel containing 10 μg/ml recombinant VEGF was transplanted. (D) Ratio of KITL-positive primordial follicles in the cultured P0 mouse ovaries. Arrows indicate primordial follicles. Mean ± SD (n = 3 for 10 μg/ml recombinant VEGF, n = 5 for control; n = 3 for 10% fetal bovine serum (FBS), n = 4 for 5% FBS and n = 7 for 0% FBS). Scale bar: 50 μm. * P
    Figure Legend Snippet: Expression of KIT ligand (KITL) in 10-week-old ICR mouse ovaries in which a biodegradable gel containing vascular endothelial growth factor (VEGF) was transplanted and in cultured P0 mouse ovaries. (A) A primordial follicle that expressed KITL (KITL-positive primordial follicles) in a 10-week-old ICR mouse ovary. (B) Primordial follicles that did not express KITL in a 10-week-old ICR mouse ovary. (C) Ratio of KITL-positive primordial follicles in the ovaries in which a biodegradable gel containing 10 μg/ml recombinant VEGF was transplanted. (D) Ratio of KITL-positive primordial follicles in the cultured P0 mouse ovaries. Arrows indicate primordial follicles. Mean ± SD (n = 3 for 10 μg/ml recombinant VEGF, n = 5 for control; n = 3 for 10% fetal bovine serum (FBS), n = 4 for 5% FBS and n = 7 for 0% FBS). Scale bar: 50 μm. * P

    Techniques Used: Expressing, Cell Culture, Recombinant

    Related Articles

    other:

    Article Title: Placenta-derived multipotent mesenchymal stromal cells: a promising potential cell-based therapy for canine inflammatory brain disease
    Article Snippet: Supernatants from LSAs co-cultures were used to measure concentrations of interleukin (IL)-2, IL-6, and IL-8; vascular endothelial growth factor (VEGF); and TNFα.

    Article Title: Anti-IL-17A treatment reduces serum inflammatory, angiogenic and tissue remodeling biomarkers accompanied by less synovial high endothelial venules in peripheral spondyloarthritis
    Article Snippet: The cytokines BMP-2, CD40 Ligand, DKK-1, CD105 (Endoglin), IL-31, IL-33, IL-6, MMP-3, Osteopontin, ROBO4, S100A8, S100A9, sclerostin (SOST), TIE-2, TNF-α, VCAM-1, Vascular Endothelial Growth Factor A (VEGF-A) were measured.

    Recombinant:

    Article Title: Novel role for SLPI in MOG-induced EAE revealed by spinal cord expression analysis
    Article Snippet: Assessment of cyclin D1 and HES1 expression in NSC and confirmation of the specificity of the effects of SLPI on NSC 100,000 NSC/well were seeded onto laminin-coated 6-well plates in 2 ml growth medium. .. After one day the specified amounts of recombinant SLPI, recombinant VEGF (R & D Systems) or recombinant α1 -antitrypsin (α1 -AT, Sigma Aldrich) were added. .. Three days later the cells were harvested, RNA was isolated, cDNA generated and RealTime-PCRs for cyclin D1 were performed with a QuantiTect-primer assay (Gene Globe, Qiagen).

    Article Title: Key endothelial cell angiogenic mechanisms are stimulated by the circulating milieu in sickle cell disease and attenuated by hydroxyurea
    Article Snippet: .. Matrigel was prepared with heparin in the absence or presence of recombinant VEGF (R & D Systems; 100 ng/mL, as previously standardized ) and 100 μM hydroxyurea before subcutaneous inoculation into mice. ..

    Article Title: Soluble VEGF receptor 1 (sFLT1) induces non-apoptotic death in ovarian and colorectal cancer cells
    Article Snippet: The cells were transfected with 50 ng of pLV-sFLT1 or pLV-EGFP as the control using Lipofectamine 2000 (Invitrogen). .. After transfection, recombinant VEGF (R & D systems, Minneapolis, Japan), rVEGFR1 (R & D systems) or bevacizumab (Chugai) was added to the culture medium and fresh medium was replaced every 3 days. .. Cell counting The cell number was evaluated to determine the effect of sFLT1 transfection.

    Article Title: Active Immunotherapy Induces Antibody Responses that Target Tumor Angiogenesis
    Article Snippet: .. For immunoblotting, 250 ng of recombinant VEGF-A and bFGF (R & D Systems) were run on a 10% reducing SDS polyacrylamide gel, transferred to a nylon membrane, probed with patient sera (1:100 dilution in 2% milk) followed by a HRP-conjugated goat anti-human IgG (Zymed) at a 1:2000 dilution, and developed with a Chemiluminescence reagent (Perkin-Elmer). .. Control anti-VEGF-A and bFGF antibodies (R & D Systems) were used at a 1:2000 dilution.

    Article Title: Glycation of vitronectin inhibits VEGF-induced angiogenesis by uncoupling VEGF receptor-2–αvβ3 integrin cross-talk
    Article Snippet: Reagents and chemicals MGO, STZ and human VN were from Sigma (St Louis, MO, USA). .. Recombinant VEGF-A was from R & D Systems (Minneapolis, MN, USA). .. Growth-factor-reduced BD Matrigel Matrix (BD Biosciences, San Jose, CA, USA) was from Chemicon International (Temecula, CA, USA).

    Mouse Assay:

    Article Title: Key endothelial cell angiogenic mechanisms are stimulated by the circulating milieu in sickle cell disease and attenuated by hydroxyurea
    Article Snippet: .. Matrigel was prepared with heparin in the absence or presence of recombinant VEGF (R & D Systems; 100 ng/mL, as previously standardized ) and 100 μM hydroxyurea before subcutaneous inoculation into mice. ..

    Transfection:

    Article Title: Soluble VEGF receptor 1 (sFLT1) induces non-apoptotic death in ovarian and colorectal cancer cells
    Article Snippet: The cells were transfected with 50 ng of pLV-sFLT1 or pLV-EGFP as the control using Lipofectamine 2000 (Invitrogen). .. After transfection, recombinant VEGF (R & D systems, Minneapolis, Japan), rVEGFR1 (R & D systems) or bevacizumab (Chugai) was added to the culture medium and fresh medium was replaced every 3 days. .. Cell counting The cell number was evaluated to determine the effect of sFLT1 transfection.

    Western Blot:

    Article Title: Pantoprazole impairs fracture healing in aged mice
    Article Snippet: .. Western blot analysisProtein expression within the callus tissue was determined by Western blot analysis, including the expression of bone morphogenetic protein-2 (BMP-2) and -4 (BMP-4), the vascular endothelial growth factor (VEGF), cysteine-rich protein (CYR) 61, receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG). ..

    Expressing:

    Article Title: Pantoprazole impairs fracture healing in aged mice
    Article Snippet: .. Western blot analysisProtein expression within the callus tissue was determined by Western blot analysis, including the expression of bone morphogenetic protein-2 (BMP-2) and -4 (BMP-4), the vascular endothelial growth factor (VEGF), cysteine-rich protein (CYR) 61, receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG). ..

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 93
    R&D Systems anti vegf bevacizumab similar antibody
    Blockade of both <t>VEGF/VEGFR2</t> and Dll4/Notch1 signaling pathways by HD105 bispecific antibody leads to inhibition of each signaling-induced cellular response. The HD105 bispecific antibody inhibited both the VEGF/VEGFR2 and the Dll4/Notch1 signaling pathways in HUVECs (A). The VEGF/VEGFR2 signaling pathway was monitored by the activation of VEGFR2 and ERK (phosphorylation). The Dll4/Notch1 signaling pathway was monitored by the generation of NICD (Notch-induced intracellular domain). HUVEC sprouting assays were performed in a fibrin gel in the presence of PBS (B), anti-VEGF <t>(bevacizumab-similar)</t> antibody (C), anti-Dll4 antibody (D), or HD105 bispecific antibody (E). Representative images show sprouting tip cells of HUVECs from the beads under basal media (B, arrowheads) and more sprouting under anti-Dll4 antibody treatment (D, arrows) but much less sprouting under anti-VEGF antibody (C) or HD105 bispecific antibody treatment (E). Scale bar (B-E), 150 μm. The bar graph (F) shows the measurement of sprouting HUVECs at 225 μm from beads (n = 20 beads/group, mean ± SE). *, P
    Anti Vegf Bevacizumab Similar Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti vegf bevacizumab similar antibody/product/R&D Systems
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti vegf bevacizumab similar antibody - by Bioz Stars, 2021-03
    93/100 stars
      Buy from Supplier

    94
    R&D Systems vegf elisa kits
    The blockade of IL-1R tI negatively impacts on leptin upregulation of <t>VEGF/VEGFR2</t> expression in 4T1 cells. Effects of leptin and IL-1R tI-blocking antibodies on levels of VEGF ( A , mRNA and C , protein) and VEGFR2 ( B , mRNA and D , protein) in 4T1 cells. Cells were incubated with leptin (0, 1.2 n) and anti mouse IL-1R tI antibody (0.1 μ g ml −1 ) for 24 h. Cells incubated with non-specific species-matched IgG2b served as negative controls. The VEGF and VEGFR2 mRNA levels were quantified by real-time RT–PCR and normalised to the glyceraldehyde-3-phosphatase dehydrogenase expression. The VEGF and VEGFR2 protein were determined by <t>ELISA</t> and western blot (WB), respectively. The VEGFR2 results from WB were analysed by densitometric analysis (imageJ software) and normalised to β -actin as a control. (a) P
    Vegf Elisa Kits, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/vegf elisa kits/product/R&D Systems
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    vegf elisa kits - by Bioz Stars, 2021-03
    94/100 stars
      Buy from Supplier

    93
    R&D Systems mouse vegf elisa kit
    NGF increased the expression of <t>VEGF</t> in Müller cells. Müller cells were treated with 100 ng/ml of nerve growth factor (NGF) compared with an equal amount of bovine serum albumin (BSA) control. After 12 or 24 h, vascular endothelial growth factor (VEGF) protein expression in the supernatants was significantly increased in the NGF-treated group according to the enzyme-linked immunosorbent assay <t>(ELISA).</t> Importantly, the VEGF increase after 24 h was significantly higher than that after the 12 h treatments. There was no statistically significant difference between 12 and 24 h in the BSA treatment group with a p value equal to 0.0644. n=6, *p
    Mouse Vegf Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse vegf elisa kit/product/R&D Systems
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse vegf elisa kit - by Bioz Stars, 2021-03
    93/100 stars
      Buy from Supplier

    93
    R&D Systems vegf sema3f recombinant protein
    <t>Sema3F</t> inhibits angiogenic sprouting of both retinal and choroidal endothelial cells. (A) Human retinal endothelial cells (HRECs) cultivated as multicellular spheroids sprout into the surrounding collagen matrix when stimulated with <t>VEGF</t> (25 ng/ml; set
    Vegf Sema3f Recombinant Protein, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/vegf sema3f recombinant protein/product/R&D Systems
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    vegf sema3f recombinant protein - by Bioz Stars, 2021-03
    93/100 stars
      Buy from Supplier

    Image Search Results


    Blockade of both VEGF/VEGFR2 and Dll4/Notch1 signaling pathways by HD105 bispecific antibody leads to inhibition of each signaling-induced cellular response. The HD105 bispecific antibody inhibited both the VEGF/VEGFR2 and the Dll4/Notch1 signaling pathways in HUVECs (A). The VEGF/VEGFR2 signaling pathway was monitored by the activation of VEGFR2 and ERK (phosphorylation). The Dll4/Notch1 signaling pathway was monitored by the generation of NICD (Notch-induced intracellular domain). HUVEC sprouting assays were performed in a fibrin gel in the presence of PBS (B), anti-VEGF (bevacizumab-similar) antibody (C), anti-Dll4 antibody (D), or HD105 bispecific antibody (E). Representative images show sprouting tip cells of HUVECs from the beads under basal media (B, arrowheads) and more sprouting under anti-Dll4 antibody treatment (D, arrows) but much less sprouting under anti-VEGF antibody (C) or HD105 bispecific antibody treatment (E). Scale bar (B-E), 150 μm. The bar graph (F) shows the measurement of sprouting HUVECs at 225 μm from beads (n = 20 beads/group, mean ± SE). *, P

    Journal: mAbs

    Article Title: Simultaneous blockade of VEGF and Dll4 by HD105, a bispecific antibody, inhibits tumor progression and angiogenesis

    doi: 10.1080/19420862.2016.1171432

    Figure Lengend Snippet: Blockade of both VEGF/VEGFR2 and Dll4/Notch1 signaling pathways by HD105 bispecific antibody leads to inhibition of each signaling-induced cellular response. The HD105 bispecific antibody inhibited both the VEGF/VEGFR2 and the Dll4/Notch1 signaling pathways in HUVECs (A). The VEGF/VEGFR2 signaling pathway was monitored by the activation of VEGFR2 and ERK (phosphorylation). The Dll4/Notch1 signaling pathway was monitored by the generation of NICD (Notch-induced intracellular domain). HUVEC sprouting assays were performed in a fibrin gel in the presence of PBS (B), anti-VEGF (bevacizumab-similar) antibody (C), anti-Dll4 antibody (D), or HD105 bispecific antibody (E). Representative images show sprouting tip cells of HUVECs from the beads under basal media (B, arrowheads) and more sprouting under anti-Dll4 antibody treatment (D, arrows) but much less sprouting under anti-VEGF antibody (C) or HD105 bispecific antibody treatment (E). Scale bar (B-E), 150 μm. The bar graph (F) shows the measurement of sprouting HUVECs at 225 μm from beads (n = 20 beads/group, mean ± SE). *, P

    Article Snippet: Increasing concentrations of anti-VEGF (bevacizumab-similar) antibody or HD105 bispecific antibody were mixed with equal volumes of His-tagged recombinant human VEGFR2/Fc (1.65 µg/ml, R & D Systems).

    Techniques: Inhibition, Activation Assay

    Suppression of tumor angiogenesis in cancer xenograft models by HD105 bispecific antibody. Fluorescence micrographs compare the vasculature of A549 human lung cancer tissues in xenograft mice after treatment with PBS (A), anti-VEGF (bevacizumab-similar) antibody (B), anti-mouse Dll4 antibody (C), or mouse HD105 bispecific antibody (D). Scale bar (A-D), 50 μm. The tumor vasculature was stained for CD31 immunoreactivity (green), and the vascular basement was stained for type IV collagen (red). Tumor vessels were decreased after treatment with anti-VEGF (bevacizumab-similar) antibody or mouse HD105 bispecific antibody, whereas tumor vessels were markedly increased after treatment with anti-mouse Dll4 antibody compared to PBS. Higher-resolution images compare the phenotype changes of tumor vessels in detail after PBS (E), anti-VEGF (bevacizumab-similar) antibody (F), anti-mouse Dll4 antibody (G), or mouse HD105 bispecific antibody treatment (H). Scale bar (E-H), 20 μm. The tumor vasculature was stained for CD31 immunoreactivity (red), and the perivascular pericyte was stained for NG2 (green). The nuclei of the tumor tissues were stained by DAPI (4′,6-diamidino-2-phenylindole). Tumor vessels after treatment with anti-mouse Dll4 antibody were conspicuously thinner and more branched than the tumor vessels of other groups. Bar graph (I) measuring tumor vessel density of A549 tumor tissues in xenograft mice confirms the conspicuous increase of tumor vessels after anti-mouse Dll4 antibody treatment but decreases after anti-VEGF (bevacizumab-similar) antibody, mouse HD105 bispecific antibody, or combination treatment with anti-mouse Dll4 antibody and anti-VEGF (bevacizumab-similar) antibody. †, P

    Journal: mAbs

    Article Title: Simultaneous blockade of VEGF and Dll4 by HD105, a bispecific antibody, inhibits tumor progression and angiogenesis

    doi: 10.1080/19420862.2016.1171432

    Figure Lengend Snippet: Suppression of tumor angiogenesis in cancer xenograft models by HD105 bispecific antibody. Fluorescence micrographs compare the vasculature of A549 human lung cancer tissues in xenograft mice after treatment with PBS (A), anti-VEGF (bevacizumab-similar) antibody (B), anti-mouse Dll4 antibody (C), or mouse HD105 bispecific antibody (D). Scale bar (A-D), 50 μm. The tumor vasculature was stained for CD31 immunoreactivity (green), and the vascular basement was stained for type IV collagen (red). Tumor vessels were decreased after treatment with anti-VEGF (bevacizumab-similar) antibody or mouse HD105 bispecific antibody, whereas tumor vessels were markedly increased after treatment with anti-mouse Dll4 antibody compared to PBS. Higher-resolution images compare the phenotype changes of tumor vessels in detail after PBS (E), anti-VEGF (bevacizumab-similar) antibody (F), anti-mouse Dll4 antibody (G), or mouse HD105 bispecific antibody treatment (H). Scale bar (E-H), 20 μm. The tumor vasculature was stained for CD31 immunoreactivity (red), and the perivascular pericyte was stained for NG2 (green). The nuclei of the tumor tissues were stained by DAPI (4′,6-diamidino-2-phenylindole). Tumor vessels after treatment with anti-mouse Dll4 antibody were conspicuously thinner and more branched than the tumor vessels of other groups. Bar graph (I) measuring tumor vessel density of A549 tumor tissues in xenograft mice confirms the conspicuous increase of tumor vessels after anti-mouse Dll4 antibody treatment but decreases after anti-VEGF (bevacizumab-similar) antibody, mouse HD105 bispecific antibody, or combination treatment with anti-mouse Dll4 antibody and anti-VEGF (bevacizumab-similar) antibody. †, P

    Article Snippet: Increasing concentrations of anti-VEGF (bevacizumab-similar) antibody or HD105 bispecific antibody were mixed with equal volumes of His-tagged recombinant human VEGFR2/Fc (1.65 µg/ml, R & D Systems).

    Techniques: Fluorescence, Mouse Assay, Staining

    Simultaneous binding to VEGF and Dll4 by HD105 bispecific antibody leads to effective blockade of VEGF/VEGFR2 and Dll4/Notch1 interactions. The HD105 bispecific antibody was constructed of the C-terminal of the anti-VEGF (bevacizumab-similar) IgG backbone linked with a single-chain Fv targeting Dll4 (A). The binding affinity of the HD105 bispecific antibody against human VEGF or human Dll4 was determined by Biacore assays (B) and ELISAs (C, D). The K D values of each antibody against VEGF or Dll4 are summarized in Table (B). The HD105 bispecific antibody (closed circle) dose-dependently bound to human VEGF (C) or Dll4 (D). In addition, the HD105 bispecific antibody simultaneously bound to each antigen, human VEGF and human Dll4, in dual-antigen capture ELISAs (E). The anti-Dll4 antibody (open circle in C) or the anti-VEGF (bevacizumab-similar) antibody (open circle in D, E) was used as negative control. Competitive ELISAs demonstrated that the HD105 bispecific antibody inhibited the interaction between VEGF/VEGFR2 (F) or Dll4/Notch1 (G) in a dose-dependent manner. The EC 50 (half maximal effective concentration) values of the anti-VEGF (bevacizumab-similar) antibody (open circle) and HD105 bispecific antibody (closed circle) for VEGF/VEGFR2 inhibition were 2.98 ± 0.5 nM and 2.84 ± 0.41 nM, respectively (F). The EC 50 values of the anti-Dll4 antibody (open circle) and HD105 bispecific antibody (closed circle) were 0.65 ± 0.06 nM and 1.14 ± 0.06 nM, respectively (G).

    Journal: mAbs

    Article Title: Simultaneous blockade of VEGF and Dll4 by HD105, a bispecific antibody, inhibits tumor progression and angiogenesis

    doi: 10.1080/19420862.2016.1171432

    Figure Lengend Snippet: Simultaneous binding to VEGF and Dll4 by HD105 bispecific antibody leads to effective blockade of VEGF/VEGFR2 and Dll4/Notch1 interactions. The HD105 bispecific antibody was constructed of the C-terminal of the anti-VEGF (bevacizumab-similar) IgG backbone linked with a single-chain Fv targeting Dll4 (A). The binding affinity of the HD105 bispecific antibody against human VEGF or human Dll4 was determined by Biacore assays (B) and ELISAs (C, D). The K D values of each antibody against VEGF or Dll4 are summarized in Table (B). The HD105 bispecific antibody (closed circle) dose-dependently bound to human VEGF (C) or Dll4 (D). In addition, the HD105 bispecific antibody simultaneously bound to each antigen, human VEGF and human Dll4, in dual-antigen capture ELISAs (E). The anti-Dll4 antibody (open circle in C) or the anti-VEGF (bevacizumab-similar) antibody (open circle in D, E) was used as negative control. Competitive ELISAs demonstrated that the HD105 bispecific antibody inhibited the interaction between VEGF/VEGFR2 (F) or Dll4/Notch1 (G) in a dose-dependent manner. The EC 50 (half maximal effective concentration) values of the anti-VEGF (bevacizumab-similar) antibody (open circle) and HD105 bispecific antibody (closed circle) for VEGF/VEGFR2 inhibition were 2.98 ± 0.5 nM and 2.84 ± 0.41 nM, respectively (F). The EC 50 values of the anti-Dll4 antibody (open circle) and HD105 bispecific antibody (closed circle) were 0.65 ± 0.06 nM and 1.14 ± 0.06 nM, respectively (G).

    Article Snippet: Increasing concentrations of anti-VEGF (bevacizumab-similar) antibody or HD105 bispecific antibody were mixed with equal volumes of His-tagged recombinant human VEGFR2/Fc (1.65 µg/ml, R & D Systems).

    Techniques: Binding Assay, Construct, Negative Control, Concentration Assay, Inhibition

    Increase in apoptotic tumor cells in cancer xenograft models treated with HD105 bispecific antibody. Fluorescence micrographs show apoptotic cells stained for activated caspase-3 antibody (red) in SCH human gastric cancer tissues in xenograft mice after treatment with PBS (A), anti-VEGF (bevacizumab-similar) antibody (B), anti-mouse Dll4 antibody (C), and mouse HD105 bispecific antibody (D and E). Scale bar (A-D), 50 μm; (E), 20 μm. Nuclei of the tumor tissues were stained by DAPI (4′,6-diamidino-2-phenylindole, blue). The higher-resolution image confirms that activated caspase-3 antibody was stained in the cytoplasm of the apoptotic cells after mouse HD105 bispecific antibody treatment (E). The bar graph (F) measuring the cell density of apoptotic cells in SCH cancer tissues confirms the significant increase in apoptotic cells after mouse HD105 bispecific antibody treatment. *, P

    Journal: mAbs

    Article Title: Simultaneous blockade of VEGF and Dll4 by HD105, a bispecific antibody, inhibits tumor progression and angiogenesis

    doi: 10.1080/19420862.2016.1171432

    Figure Lengend Snippet: Increase in apoptotic tumor cells in cancer xenograft models treated with HD105 bispecific antibody. Fluorescence micrographs show apoptotic cells stained for activated caspase-3 antibody (red) in SCH human gastric cancer tissues in xenograft mice after treatment with PBS (A), anti-VEGF (bevacizumab-similar) antibody (B), anti-mouse Dll4 antibody (C), and mouse HD105 bispecific antibody (D and E). Scale bar (A-D), 50 μm; (E), 20 μm. Nuclei of the tumor tissues were stained by DAPI (4′,6-diamidino-2-phenylindole, blue). The higher-resolution image confirms that activated caspase-3 antibody was stained in the cytoplasm of the apoptotic cells after mouse HD105 bispecific antibody treatment (E). The bar graph (F) measuring the cell density of apoptotic cells in SCH cancer tissues confirms the significant increase in apoptotic cells after mouse HD105 bispecific antibody treatment. *, P

    Article Snippet: Increasing concentrations of anti-VEGF (bevacizumab-similar) antibody or HD105 bispecific antibody were mixed with equal volumes of His-tagged recombinant human VEGFR2/Fc (1.65 µg/ml, R & D Systems).

    Techniques: Fluorescence, Staining, Mouse Assay

    The blockade of IL-1R tI negatively impacts on leptin upregulation of VEGF/VEGFR2 expression in 4T1 cells. Effects of leptin and IL-1R tI-blocking antibodies on levels of VEGF ( A , mRNA and C , protein) and VEGFR2 ( B , mRNA and D , protein) in 4T1 cells. Cells were incubated with leptin (0, 1.2 n) and anti mouse IL-1R tI antibody (0.1 μ g ml −1 ) for 24 h. Cells incubated with non-specific species-matched IgG2b served as negative controls. The VEGF and VEGFR2 mRNA levels were quantified by real-time RT–PCR and normalised to the glyceraldehyde-3-phosphatase dehydrogenase expression. The VEGF and VEGFR2 protein were determined by ELISA and western blot (WB), respectively. The VEGFR2 results from WB were analysed by densitometric analysis (imageJ software) and normalised to β -actin as a control. (a) P

    Journal: British Journal of Cancer

    Article Title: Leptin pro-angiogenic signature in breast cancer is linked to IL-1 signalling

    doi: 10.1038/sj.bjc.6606013

    Figure Lengend Snippet: The blockade of IL-1R tI negatively impacts on leptin upregulation of VEGF/VEGFR2 expression in 4T1 cells. Effects of leptin and IL-1R tI-blocking antibodies on levels of VEGF ( A , mRNA and C , protein) and VEGFR2 ( B , mRNA and D , protein) in 4T1 cells. Cells were incubated with leptin (0, 1.2 n) and anti mouse IL-1R tI antibody (0.1 μ g ml −1 ) for 24 h. Cells incubated with non-specific species-matched IgG2b served as negative controls. The VEGF and VEGFR2 mRNA levels were quantified by real-time RT–PCR and normalised to the glyceraldehyde-3-phosphatase dehydrogenase expression. The VEGF and VEGFR2 protein were determined by ELISA and western blot (WB), respectively. The VEGFR2 results from WB were analysed by densitometric analysis (imageJ software) and normalised to β -actin as a control. (a) P

    Article Snippet: Reagents and antibodies Recombinant mouse leptin and mouse IL-1β , IL-1α , IL-1Ra and VEGF ELISA Kits were from R & D Systems (Minneapolis, MN, USA).

    Techniques: Expressing, Blocking Assay, Incubation, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Western Blot, Software

    NGF increased the expression of VEGF in Müller cells. Müller cells were treated with 100 ng/ml of nerve growth factor (NGF) compared with an equal amount of bovine serum albumin (BSA) control. After 12 or 24 h, vascular endothelial growth factor (VEGF) protein expression in the supernatants was significantly increased in the NGF-treated group according to the enzyme-linked immunosorbent assay (ELISA). Importantly, the VEGF increase after 24 h was significantly higher than that after the 12 h treatments. There was no statistically significant difference between 12 and 24 h in the BSA treatment group with a p value equal to 0.0644. n=6, *p

    Journal: Molecular Vision

    Article Title: NGF increases VEGF expression and promotes cell proliferation via ERK1/2 and AKT signaling in Müller cells

    doi:

    Figure Lengend Snippet: NGF increased the expression of VEGF in Müller cells. Müller cells were treated with 100 ng/ml of nerve growth factor (NGF) compared with an equal amount of bovine serum albumin (BSA) control. After 12 or 24 h, vascular endothelial growth factor (VEGF) protein expression in the supernatants was significantly increased in the NGF-treated group according to the enzyme-linked immunosorbent assay (ELISA). Importantly, the VEGF increase after 24 h was significantly higher than that after the 12 h treatments. There was no statistically significant difference between 12 and 24 h in the BSA treatment group with a p value equal to 0.0644. n=6, *p

    Article Snippet: VEGF detection with ELISA and Müller cell proliferation with MTT assay The Müller cells seeded on 24-well or 96-well plates (Corning Inc., Corning, NY) were cultured in serum-free DMEM/F12 overnight and then treated with 100 ng/ml BSA, 100 ng/ml of recombinant NGF with or without K252a, U0126, and LY294002 for 12, 24, 48, and 72 h. At the appropriate time points, the supernatants of the treated Müller cells were collected, and VEGF levels were detected with a mouse VEGF ELISA kit (R & D Systems, Minneapolis, MN) according to the manufacturer’s instructions.

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay

    NGF increases VEGF expression via the TrkA receptor and is mediated by the activation of ERK1/2 and AKT signaling. Müller cells were treated with 100 ng/ml of nerve growth factor (NGF) with or without 20 nM K252a (TrkA inhibitor), 10 µM U0126 (extracellular signal-regulated kinases 1/2 (ERK1/2) pathway inhibitor), or 10 µM LY294002 (phosphatidylinositol 3-kinase (PI3K)/AKT inhibitor) for 12 or 24 h. The vascular endothelial growth factor (VEGF) protein level in the supernatants was detected with enzyme-linked immunosorbent assay (ELISA). The TrkA, ERK1/2, and PI3K/AKT inhibitors decreased the ability of NGF to promote VEGF expression to some extent. n=6, * p

    Journal: Molecular Vision

    Article Title: NGF increases VEGF expression and promotes cell proliferation via ERK1/2 and AKT signaling in Müller cells

    doi:

    Figure Lengend Snippet: NGF increases VEGF expression via the TrkA receptor and is mediated by the activation of ERK1/2 and AKT signaling. Müller cells were treated with 100 ng/ml of nerve growth factor (NGF) with or without 20 nM K252a (TrkA inhibitor), 10 µM U0126 (extracellular signal-regulated kinases 1/2 (ERK1/2) pathway inhibitor), or 10 µM LY294002 (phosphatidylinositol 3-kinase (PI3K)/AKT inhibitor) for 12 or 24 h. The vascular endothelial growth factor (VEGF) protein level in the supernatants was detected with enzyme-linked immunosorbent assay (ELISA). The TrkA, ERK1/2, and PI3K/AKT inhibitors decreased the ability of NGF to promote VEGF expression to some extent. n=6, * p

    Article Snippet: VEGF detection with ELISA and Müller cell proliferation with MTT assay The Müller cells seeded on 24-well or 96-well plates (Corning Inc., Corning, NY) were cultured in serum-free DMEM/F12 overnight and then treated with 100 ng/ml BSA, 100 ng/ml of recombinant NGF with or without K252a, U0126, and LY294002 for 12, 24, 48, and 72 h. At the appropriate time points, the supernatants of the treated Müller cells were collected, and VEGF levels were detected with a mouse VEGF ELISA kit (R & D Systems, Minneapolis, MN) according to the manufacturer’s instructions.

    Techniques: Expressing, Activation Assay, Enzyme-linked Immunosorbent Assay

    Sema3F inhibits angiogenic sprouting of both retinal and choroidal endothelial cells. (A) Human retinal endothelial cells (HRECs) cultivated as multicellular spheroids sprout into the surrounding collagen matrix when stimulated with VEGF (25 ng/ml; set

    Journal: FEBS letters

    Article Title: Semaphorin 3F forms an anti-angiogenic barrier in outer retina

    doi: 10.1016/j.febslet.2013.04.008

    Figure Lengend Snippet: Sema3F inhibits angiogenic sprouting of both retinal and choroidal endothelial cells. (A) Human retinal endothelial cells (HRECs) cultivated as multicellular spheroids sprout into the surrounding collagen matrix when stimulated with VEGF (25 ng/ml; set

    Article Snippet: Freshly prepared gels were transferred rapidly into a humidified incubator (37 °C, 5% CO2 ), and after the gels had solidified, 0.1 ml of serum-free medium (Cell Systems) was added per well containing VEGF ± Sema3F recombinant protein (RnD Systems).

    Techniques: