Structured Review

R&D Systems vegf a 165
MMP-1-PAR1 stimulates secretion of CXCR1/2 chemokines from ovarian carcinoma cells. A , OVCAR-4 cells were stimulated with either 1 nM MMP-1 or PBS buffer in RPMI with 0.1% BSA and conditioned media (CM) was collected after 18 h. The angiogenesis array membranes were incubated with CM from the OVCAR-4 cells and fold change of the spot intensities was quantified using NIH ImageJ software. B ) in OVCAR-4, IGROV-1, OVCAR-3 and OVCAR-4/PAR1 shRNAi ovarian carcinoma cell lines. C–E, ELISA analysis was used to measure IL-8 (C), GRO-α (D), and <t>VEGF-A-165</t> (E) levels in CM from various ovarian carcinoma cell lines that were stimulated with 1 nM MMP-1 in the presence or absence of the PAR1 antagonist pepducin P1pal-7 (3 μM), the small molecule PAR1 antagonist RWJ-56110 (5 μM), or buffer control as indicated. Data (mean ± SE) are from 2–4 experiments performed in duplicate.
Vegf A 165, 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
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1) Product Images from "Identification of a metalloprotease-chemokine signaling system in the ovarian cancer microenvironment: implications for anti-angiogenic therapy"

Article Title: Identification of a metalloprotease-chemokine signaling system in the ovarian cancer microenvironment: implications for anti-angiogenic therapy

Journal: Cancer research

doi: 10.1158/0008-5472.CAN-09-4341

MMP-1-PAR1 stimulates secretion of CXCR1/2 chemokines from ovarian carcinoma cells. A , OVCAR-4 cells were stimulated with either 1 nM MMP-1 or PBS buffer in RPMI with 0.1% BSA and conditioned media (CM) was collected after 18 h. The angiogenesis array membranes were incubated with CM from the OVCAR-4 cells and fold change of the spot intensities was quantified using NIH ImageJ software. B ) in OVCAR-4, IGROV-1, OVCAR-3 and OVCAR-4/PAR1 shRNAi ovarian carcinoma cell lines. C–E, ELISA analysis was used to measure IL-8 (C), GRO-α (D), and VEGF-A-165 (E) levels in CM from various ovarian carcinoma cell lines that were stimulated with 1 nM MMP-1 in the presence or absence of the PAR1 antagonist pepducin P1pal-7 (3 μM), the small molecule PAR1 antagonist RWJ-56110 (5 μM), or buffer control as indicated. Data (mean ± SE) are from 2–4 experiments performed in duplicate.
Figure Legend Snippet: MMP-1-PAR1 stimulates secretion of CXCR1/2 chemokines from ovarian carcinoma cells. A , OVCAR-4 cells were stimulated with either 1 nM MMP-1 or PBS buffer in RPMI with 0.1% BSA and conditioned media (CM) was collected after 18 h. The angiogenesis array membranes were incubated with CM from the OVCAR-4 cells and fold change of the spot intensities was quantified using NIH ImageJ software. B ) in OVCAR-4, IGROV-1, OVCAR-3 and OVCAR-4/PAR1 shRNAi ovarian carcinoma cell lines. C–E, ELISA analysis was used to measure IL-8 (C), GRO-α (D), and VEGF-A-165 (E) levels in CM from various ovarian carcinoma cell lines that were stimulated with 1 nM MMP-1 in the presence or absence of the PAR1 antagonist pepducin P1pal-7 (3 μM), the small molecule PAR1 antagonist RWJ-56110 (5 μM), or buffer control as indicated. Data (mean ± SE) are from 2–4 experiments performed in duplicate.

Techniques Used: Incubation, Software, Enzyme-linked Immunosorbent Assay

Related Articles

other:

Article Title: Growth Factor–like Gene Regulation Is Separable from Survival and Maturation in Antibody-Secreting Cells
Article Snippet: For cytokine combination experiments and TGF-β3 dose response, cells were seeded at 5 × 105 per ml in media supplemented with IL-6 (10 ng/ml), IL-21 (50 ng/ml), IFN-α (100 U/ml), and combinations of Jagged 1 (2 μg/ml); Osteopontin (1 μg/ml); Osteoprotegerin, SCF, and IGF-BP2 (100 ng/ml); Activin A, and M-CSF (50 ng/ml); IGF-II (30 ng/ml): ANGPT1, VEGF-165, VEGF-121, MIF, and TGF-β3 (10 ng/ml or 0.1–1000 ng/ml for dose response).

Article Title: Heparan sulfate functions are altered in the osteoarthritic cartilage
Article Snippet: Then, HBP were added to each well (FGF2 at 2.5 ng/well; VEGF-165 at 5 ng/well) together with increasing concentrations of GAG extracted from the samples (serial dilutions from 0.01 to 10 μg/mL in PBS) in duplicate.

Article Title: Fatty acid binding protein 4 is a target of VEGF and a regulator of cell proliferation in endothelial cells
Article Snippet: VEGF-A 165 (VEGF) and human basic FGF (bFGF) were purchased from R & D Systems (Minneapolis, MN, USA) and Neuromics (Edina, MN, USA), respectively.

Article Title: Dual role of fatty acid-binding protein 5 on endothelial cell fate: a potential link between lipid metabolism and angiogenic responses
Article Snippet: In some experiments, cells were treated with VEGF-A 165 (R & D Systems, Minneapolis, MN) or chemically defined lipid mixture 1 (Sigma).

Recombinant:

Article Title: Endothelial cell-fatty acid binding protein 4 promotes angiogenesis: role of stem cell factor/c-kit pathway
Article Snippet: HEK-293T cells (ATCC, Rockville, MD, USA) were cultured in DMEM (Invitrogen) supplemented with 10 % FBS and 1× non-essential amino acids (Sigma). .. VEGF-A 165 (VEGF), mouse basic FGF (bFGF), and recombinant stem cell factor (SCF) were purchased from R & D Systems (Minneapolis, MN, USA). .. LY294002, Wortmannin, SB203580, L-NAME, and Rapamycin were purchased from Calbiochem (San Diego, CA, USA).

Article Title: Dll4-containing exosomes induce capillary sprout retraction in a 3D microenvironment
Article Snippet: We transduced U-87 tumor cell line with human Dll4 in pLVX-IRES-ZsGreen lentiviral vector to overexpress Dll4. .. Recombinant human Dll4 and VEGF-165 were purchased from R & D Systems. .. Microfluidic device design Microfluidic devices (MFDs) were fabricated from polydimethylsiloxane (PDMS – Dow Corning Sylgard 184) using standard soft lithography and plasma bonded to glass cover slip ( ).

Incubation:

Article Title: Granzyme B Releases Vascular Endothelial Growth Factor from Extracellular Matrix and Induces Vascular Permeability
Article Snippet: .. VEGF 165 (50ng/ml) (R & D systems, Minneapolis, MN) was added to the FN coated wells and incubated for 2 h at 37°C followed by extensive washing to remove unbound VEGF. .. Human purified GZMB (50 nM) (Axxora, San Diego, CA) in Tris buffer (50mM Tris, pH=7.4) with either vehicle control (1:100 DMSO) or GZMB inhibitor (Compound 20 (50μM), UBC Centre for Drug Research and Development, Vancouver, BC) [ ] were added to the well for additional 2 h at 37°C.

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    R&D Systems recombinant human vascular endothelial growth factor
    Model for the role of the Abl family kinases in signaling pathways regulating <t>endothelial</t> permeability. The Abl and Arg kinases are activated in endothelial cells downstream of receptors for the permeability-inducing factors VEGF, thrombin, and histamine. VEGF-mediated Abl kinase activation requires Src family kinase activity. The Abl kinases positively regulate phosphorylation of MLC2 (S19) in response to these permeability-inducing agonists, likely through regulating the activity of Ca 2+ /calmodulin-dependent targets such as MLCK. Abl kinase activity is required for maximal Ca 2+ mobilization in response to stimulation with permeability-inducing factors. The Abl kinases additionally modulate VEGF-induced phosphorylation of VEGFR2 at Y1175, which regulates downstream PLCγ activation, IP 3 generation, and ER Ca 2+ release. Abl kinases promote Ca 2+ mobilization by thrombin and histamine by mechanisms yet to be characterized. Abl kinases negatively regulate basal activity levels of the Rac1 and Rap1 GTPases, which have been shown to support endothelial barrier function by promoting cortical actin deposition and adherens junction stability. Abbreviations: EC, endothelial cell; VEGF, <t>vascular</t> endothelial <t>growth</t> <t>factor;</t> VEGFR2, VEGF receptor 2; Y, tyrosine; PAR-1, protease-activated receptor 1 (thrombin); H1, histamine H1 receptor; MLC2, myosin regulatory light chain; S, serine; MLCK, myosin light chain kinase; PLC, phospholipase C; IP 3 , inositol-1,4,5-trisphosphate; IP 3 R, IP 3 receptor; ER, endoplasmic reticulum.
    Recombinant Human Vascular Endothelial Growth Factor, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems recombinant human vegf165
    Endothelial cell proliferation by VEGF189 and <t>VEGF165</t> produced by selected MDA-MB-231 cells. HUVECs (5 × 10 3 /well) were incubated with the conditioned medium of selected V165 and V189 clones, as described in Materials and Methods; the proliferation
    Recombinant Human Vegf165, 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
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    93
    R&D Systems vegf 165
    APLNR regulates  CXCR4  expression through miR-139-5p. ( a , b ) CXCR4 expression in response to shear stress exposure in HUVECs, with or without concurrent  APLNR  knockdown. mRNA ( a ) and protein levels ( b ) are shown. ( c ) CXCR4 expression in response to  AGO2  knockdown. ( d ) CXCR4 expression in response to shear stress exposure in HUVECs, with or without concurrent  AGO2  knockdown. ( e ) Determination of miR-139-5p levels in FACS sorted ECs from P5 retinas of  Aplnr −/− ,  Apln −/−  mice and respective littermates.  n= 3 retinas per genotype. ( f ) CXCR4 expression in HUVECs overexpressing miR-139-5p mimic or non-targeting control anti-miR. ( g ) Expression levels of miR-139-5p in response to shear stress, with or without concurrent  APLNR  knockdown. ( h ) CXCR4 expression in HUVECs in response to shear stress exposure, with or without concurrent miR-139-5p inhibition via anti-miR. ( i ) Sprouting assay using HUVEC covered beads transduced with miR-139-5p or control lentivirus in response to SDF-1α or VEGF 165. Scale bar, 175 μm. ( j ) Migration assay of HUVECs transduced with miR-139-5p or control lentivirus in response to SDF-1α. Scale bar, 200 μm. * P
    Vegf 165, 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
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    The Recombinant Zebrafish VEGF 165 Protein from R D Systems is derived from Sf 21 stably transfected The Recombinant Zebrafish VEGF 165 Protein has been validated for the following applications
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    Model for the role of the Abl family kinases in signaling pathways regulating endothelial permeability. The Abl and Arg kinases are activated in endothelial cells downstream of receptors for the permeability-inducing factors VEGF, thrombin, and histamine. VEGF-mediated Abl kinase activation requires Src family kinase activity. The Abl kinases positively regulate phosphorylation of MLC2 (S19) in response to these permeability-inducing agonists, likely through regulating the activity of Ca 2+ /calmodulin-dependent targets such as MLCK. Abl kinase activity is required for maximal Ca 2+ mobilization in response to stimulation with permeability-inducing factors. The Abl kinases additionally modulate VEGF-induced phosphorylation of VEGFR2 at Y1175, which regulates downstream PLCγ activation, IP 3 generation, and ER Ca 2+ release. Abl kinases promote Ca 2+ mobilization by thrombin and histamine by mechanisms yet to be characterized. Abl kinases negatively regulate basal activity levels of the Rac1 and Rap1 GTPases, which have been shown to support endothelial barrier function by promoting cortical actin deposition and adherens junction stability. Abbreviations: EC, endothelial cell; VEGF, vascular endothelial growth factor; VEGFR2, VEGF receptor 2; Y, tyrosine; PAR-1, protease-activated receptor 1 (thrombin); H1, histamine H1 receptor; MLC2, myosin regulatory light chain; S, serine; MLCK, myosin light chain kinase; PLC, phospholipase C; IP 3 , inositol-1,4,5-trisphosphate; IP 3 R, IP 3 receptor; ER, endoplasmic reticulum.

    Journal: PLoS ONE

    Article Title: Abl Family Kinases Regulate Endothelial Barrier Function In Vitro and in Mice

    doi: 10.1371/journal.pone.0085231

    Figure Lengend Snippet: Model for the role of the Abl family kinases in signaling pathways regulating endothelial permeability. The Abl and Arg kinases are activated in endothelial cells downstream of receptors for the permeability-inducing factors VEGF, thrombin, and histamine. VEGF-mediated Abl kinase activation requires Src family kinase activity. The Abl kinases positively regulate phosphorylation of MLC2 (S19) in response to these permeability-inducing agonists, likely through regulating the activity of Ca 2+ /calmodulin-dependent targets such as MLCK. Abl kinase activity is required for maximal Ca 2+ mobilization in response to stimulation with permeability-inducing factors. The Abl kinases additionally modulate VEGF-induced phosphorylation of VEGFR2 at Y1175, which regulates downstream PLCγ activation, IP 3 generation, and ER Ca 2+ release. Abl kinases promote Ca 2+ mobilization by thrombin and histamine by mechanisms yet to be characterized. Abl kinases negatively regulate basal activity levels of the Rac1 and Rap1 GTPases, which have been shown to support endothelial barrier function by promoting cortical actin deposition and adherens junction stability. Abbreviations: EC, endothelial cell; VEGF, vascular endothelial growth factor; VEGFR2, VEGF receptor 2; Y, tyrosine; PAR-1, protease-activated receptor 1 (thrombin); H1, histamine H1 receptor; MLC2, myosin regulatory light chain; S, serine; MLCK, myosin light chain kinase; PLC, phospholipase C; IP 3 , inositol-1,4,5-trisphosphate; IP 3 R, IP 3 receptor; ER, endoplasmic reticulum.

    Article Snippet: Recombinant human vascular endothelial growth factor (VEGF-A-165) was purchased from R & D Systems.

    Techniques: Permeability, Activation Assay, Activity Assay, Planar Chromatography

    Endothelial cell proliferation by VEGF189 and VEGF165 produced by selected MDA-MB-231 cells. HUVECs (5 × 10 3 /well) were incubated with the conditioned medium of selected V165 and V189 clones, as described in Materials and Methods; the proliferation

    Journal: The American Journal of Pathology

    Article Title: Overexpression of Vascular Endothelial Growth Factor 189 in Breast Cancer Cells Leads to Delayed Tumor Uptake with Dilated Intratumoral Vessels

    doi: 10.2353/ajpath.2008.070181

    Figure Lengend Snippet: Endothelial cell proliferation by VEGF189 and VEGF165 produced by selected MDA-MB-231 cells. HUVECs (5 × 10 3 /well) were incubated with the conditioned medium of selected V165 and V189 clones, as described in Materials and Methods; the proliferation

    Article Snippet: Recombinant human VEGF165 (R & D Systems) and VEGF189 were used as controls.

    Techniques: Produced, Multiple Displacement Amplification, Incubation, Clone Assay

    Generation of MDA-MB-231 Cells Stably Expressing VEGF189 or VEGF165 Protein

    Journal: The American Journal of Pathology

    Article Title: Overexpression of Vascular Endothelial Growth Factor 189 in Breast Cancer Cells Leads to Delayed Tumor Uptake with Dilated Intratumoral Vessels

    doi: 10.2353/ajpath.2008.070181

    Figure Lengend Snippet: Generation of MDA-MB-231 Cells Stably Expressing VEGF189 or VEGF165 Protein

    Article Snippet: Recombinant human VEGF165 (R & D Systems) and VEGF189 were used as controls.

    Techniques: Multiple Displacement Amplification, Stable Transfection, Expressing

    Growth curves of MDA-overexpressing VEGF189 and VEGF165 tumors induced in SCID mice. Cells (5 × 10 6 ) were subcutaneously injected in SCID mice as described in Materials and Methods. A: Tumors were generated from V189-13 or V165-42 clone, or cV

    Journal: The American Journal of Pathology

    Article Title: Overexpression of Vascular Endothelial Growth Factor 189 in Breast Cancer Cells Leads to Delayed Tumor Uptake with Dilated Intratumoral Vessels

    doi: 10.2353/ajpath.2008.070181

    Figure Lengend Snippet: Growth curves of MDA-overexpressing VEGF189 and VEGF165 tumors induced in SCID mice. Cells (5 × 10 6 ) were subcutaneously injected in SCID mice as described in Materials and Methods. A: Tumors were generated from V189-13 or V165-42 clone, or cV

    Article Snippet: Recombinant human VEGF165 (R & D Systems) and VEGF189 were used as controls.

    Techniques: Multiple Displacement Amplification, Mouse Assay, Injection, Generated

    In Vitro Tube Formation Assay Using Human Umbilical Vein Endothelial Cells (HUVECs) on a Three-Dimensional Gel Consisting of Diluted Matrigel The cells were treated with Apt01 (10 μM), Apt02 (10 μM), or VEGF165 (10 ng/mL, 0.26 nM) for 24 h. (A) Representative images of tube formation of HUVECs on Matrigel, which are treated by aptamers or VEGF165. Scale bars, 1 mm. (B) Time course of mesh number in the images of the HUVEC networks at 4, 7, and 24 h. Error bars represent standard deviation of the mean (n = 3 plots). (C–E) Boxplot showing mesh number in the images of the HUVEC networks at (C) 4, (D) 7, and (E) 24 h (n = 3 plots). *p

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: Binding and Structural Properties of DNA Aptamers with VEGF-A-Mimic Activity

    doi: 10.1016/j.omtn.2019.12.034

    Figure Lengend Snippet: In Vitro Tube Formation Assay Using Human Umbilical Vein Endothelial Cells (HUVECs) on a Three-Dimensional Gel Consisting of Diluted Matrigel The cells were treated with Apt01 (10 μM), Apt02 (10 μM), or VEGF165 (10 ng/mL, 0.26 nM) for 24 h. (A) Representative images of tube formation of HUVECs on Matrigel, which are treated by aptamers or VEGF165. Scale bars, 1 mm. (B) Time course of mesh number in the images of the HUVEC networks at 4, 7, and 24 h. Error bars represent standard deviation of the mean (n = 3 plots). (C–E) Boxplot showing mesh number in the images of the HUVEC networks at (C) 4, (D) 7, and (E) 24 h (n = 3 plots). *p

    Article Snippet: HUVECs (1.1 × 105 cells/well) were placed into 24-well flat-bottomed plates pre-coated with Matrigel and then incubated with aptamers (10 μM) or VEGF165 (Recombinant Human VEGF 165 Protein, Cat. No. 293-VE [R & D Systems, USA]; 10 ng/mL, 0.26 nM) for 24 h. In the experiment of dose dependency, the Apt02 concentration of more than 10 μM showed the significant difference from control group (data not shown).

    Techniques: In Vitro, Tube Formation Assay, Standard Deviation

    APLNR regulates  CXCR4  expression through miR-139-5p. ( a , b ) CXCR4 expression in response to shear stress exposure in HUVECs, with or without concurrent  APLNR  knockdown. mRNA ( a ) and protein levels ( b ) are shown. ( c ) CXCR4 expression in response to  AGO2  knockdown. ( d ) CXCR4 expression in response to shear stress exposure in HUVECs, with or without concurrent  AGO2  knockdown. ( e ) Determination of miR-139-5p levels in FACS sorted ECs from P5 retinas of  Aplnr −/− ,  Apln −/−  mice and respective littermates.  n= 3 retinas per genotype. ( f ) CXCR4 expression in HUVECs overexpressing miR-139-5p mimic or non-targeting control anti-miR. ( g ) Expression levels of miR-139-5p in response to shear stress, with or without concurrent  APLNR  knockdown. ( h ) CXCR4 expression in HUVECs in response to shear stress exposure, with or without concurrent miR-139-5p inhibition via anti-miR. ( i ) Sprouting assay using HUVEC covered beads transduced with miR-139-5p or control lentivirus in response to SDF-1α or VEGF 165. Scale bar, 175 μm. ( j ) Migration assay of HUVECs transduced with miR-139-5p or control lentivirus in response to SDF-1α. Scale bar, 200 μm. * P

    Journal: Nature Communications

    Article Title: MicroRNA 139-5p coordinates APLNR-CXCR4 crosstalk during vascular maturation

    doi: 10.1038/ncomms11268

    Figure Lengend Snippet: APLNR regulates CXCR4 expression through miR-139-5p. ( a , b ) CXCR4 expression in response to shear stress exposure in HUVECs, with or without concurrent APLNR knockdown. mRNA ( a ) and protein levels ( b ) are shown. ( c ) CXCR4 expression in response to AGO2 knockdown. ( d ) CXCR4 expression in response to shear stress exposure in HUVECs, with or without concurrent AGO2 knockdown. ( e ) Determination of miR-139-5p levels in FACS sorted ECs from P5 retinas of Aplnr −/− , Apln −/− mice and respective littermates. n= 3 retinas per genotype. ( f ) CXCR4 expression in HUVECs overexpressing miR-139-5p mimic or non-targeting control anti-miR. ( g ) Expression levels of miR-139-5p in response to shear stress, with or without concurrent APLNR knockdown. ( h ) CXCR4 expression in HUVECs in response to shear stress exposure, with or without concurrent miR-139-5p inhibition via anti-miR. ( i ) Sprouting assay using HUVEC covered beads transduced with miR-139-5p or control lentivirus in response to SDF-1α or VEGF 165. Scale bar, 175 μm. ( j ) Migration assay of HUVECs transduced with miR-139-5p or control lentivirus in response to SDF-1α. Scale bar, 200 μm. * P

    Article Snippet: The fibrinogen/bead solution was allowed to clot for 5 min at room temperature and then at 37 °C in 5% CO2 for 15 min. EGM-2 containing 50 ng ml−1 SDF-1α (SRP3252, Sigma-Aldrich), or 20 ng ml−1 VEGF 165 (293-VE, R & D Systems) was used.

    Techniques: Expressing, FACS, Mouse Assay, Inhibition, Transduction, Migration