vegf elisa kits  (R&D Systems)

 
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    Name:
    Mouse VEGF D Antibody
    Description:
    The Mouse VEGF D Antibody from R D Systems is a rat monoclonal antibody to VEGF D This antibody reacts with mouse The Mouse VEGF D Antibody has been validated for the following applications Western Blot ELISA Capture Matched Antibody Pair
    Catalog Number:
    MAB469-SP
    Price:
    99
    Category:
    Primary Antibodies
    Applications:
    Western Blot, ELISA Capture (Matched Antibody Pair)
    Purity:
    Protein A or G purified from hybridoma culture supernatant
    Conjugate:
    Unconjugated
    Immunogen:
    E. coli-derived recombinant mouse VEGF-D, Phe98-Ser206, Accession # P97946
    Size:
    25 ug
    Host:
    Rat
    Isotype:
    IgG2a
    Buy from Supplier


    Structured Review

    R&D Systems vegf elisa kits
    a) MC3T3-E1 cells were cultured with conditioned medium derived from FW-stimulated or -unstimulated HeLa cells for 1 h and further cultured with fresh 10% FCS-αMEM for 24 h. The culture supernatants were harvested and subjected to IL-6 (left) and <t>VEGF</t> (right) <t>ELISA.</t> The MC3T3-E1 cells were cultured with b) rh bFGF at concentrations of 0, 0.01, 0.1, 1, 3 and 10 nM (IL-6, left) or 0, 1, 3 and 10 nM (VEGF, right) for 1 h. The cells were cultured with c) EMMPRIN at concentrations of 0, 0.5, 1 and 2 µg/ml (IL-6, left) or 0, 0.5, 1 and 2 µg/ml (VEGF, right) for 1 h. The medium was exchanged after 1h of stimulation, and the cells were incubated for 24 h. Culture supernatants were harvested and subjected to IL-6 ELISA. The mean of at least four independent experiments are shown. *p
    The Mouse VEGF D Antibody from R D Systems is a rat monoclonal antibody to VEGF D This antibody reacts with mouse The Mouse VEGF D Antibody has been validated for the following applications Western Blot ELISA Capture Matched Antibody Pair
    https://www.bioz.com/result/vegf elisa kits/product/R&D Systems
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    vegf elisa kits - by Bioz Stars, 2021-04
    97/100 stars

    Images

    1) Product Images from "EMMPRIN Inhibits bFGF-Induced IL-6 Secretion in an Osteoblastic Cell Line, MC3T3-E1"

    Article Title: EMMPRIN Inhibits bFGF-Induced IL-6 Secretion in an Osteoblastic Cell Line, MC3T3-E1

    Journal: International Journal of Medical Sciences

    doi: 10.7150/ijms.20387

    a) MC3T3-E1 cells were cultured with conditioned medium derived from FW-stimulated or -unstimulated HeLa cells for 1 h and further cultured with fresh 10% FCS-αMEM for 24 h. The culture supernatants were harvested and subjected to IL-6 (left) and VEGF (right) ELISA. The MC3T3-E1 cells were cultured with b) rh bFGF at concentrations of 0, 0.01, 0.1, 1, 3 and 10 nM (IL-6, left) or 0, 1, 3 and 10 nM (VEGF, right) for 1 h. The cells were cultured with c) EMMPRIN at concentrations of 0, 0.5, 1 and 2 µg/ml (IL-6, left) or 0, 0.5, 1 and 2 µg/ml (VEGF, right) for 1 h. The medium was exchanged after 1h of stimulation, and the cells were incubated for 24 h. Culture supernatants were harvested and subjected to IL-6 ELISA. The mean of at least four independent experiments are shown. *p
    Figure Legend Snippet: a) MC3T3-E1 cells were cultured with conditioned medium derived from FW-stimulated or -unstimulated HeLa cells for 1 h and further cultured with fresh 10% FCS-αMEM for 24 h. The culture supernatants were harvested and subjected to IL-6 (left) and VEGF (right) ELISA. The MC3T3-E1 cells were cultured with b) rh bFGF at concentrations of 0, 0.01, 0.1, 1, 3 and 10 nM (IL-6, left) or 0, 1, 3 and 10 nM (VEGF, right) for 1 h. The cells were cultured with c) EMMPRIN at concentrations of 0, 0.5, 1 and 2 µg/ml (IL-6, left) or 0, 0.5, 1 and 2 µg/ml (VEGF, right) for 1 h. The medium was exchanged after 1h of stimulation, and the cells were incubated for 24 h. Culture supernatants were harvested and subjected to IL-6 ELISA. The mean of at least four independent experiments are shown. *p

    Techniques Used: Cell Culture, Derivative Assay, Enzyme-linked Immunosorbent Assay, Incubation

    2) Product Images from "Large adipose tissue generation in a mussel-inspired bioreactor of elastic–mimetic cryogel and platelets"

    Article Title: Large adipose tissue generation in a mussel-inspired bioreactor of elastic–mimetic cryogel and platelets

    Journal: Journal of Tissue Engineering

    doi: 10.1177/2041731418808633

    Growth factors release by the pDA/GC/Plt system. PDGF (a) and VEGF (b) were detected with ELISA. The release was prolonged in the pDA/GC/Plt group compared to that in the PRP group. A significant difference was observed after 3 h for both PDGF and VEGF. Chamber fluid was extracted and tested by ELISA for PDGF (c) and VEGF (d). pDA/GC/Plt incorporated into the TEC had significantly higher levels of PDGF and VEGF from days 7 and 3, respectively (p
    Figure Legend Snippet: Growth factors release by the pDA/GC/Plt system. PDGF (a) and VEGF (b) were detected with ELISA. The release was prolonged in the pDA/GC/Plt group compared to that in the PRP group. A significant difference was observed after 3 h for both PDGF and VEGF. Chamber fluid was extracted and tested by ELISA for PDGF (c) and VEGF (d). pDA/GC/Plt incorporated into the TEC had significantly higher levels of PDGF and VEGF from days 7 and 3, respectively (p

    Techniques Used: Enzyme-linked Immunosorbent Assay

    3) Product Images from "Large adipose tissue generation in a mussel-inspired bioreactor of elastic–mimetic cryogel and platelets"

    Article Title: Large adipose tissue generation in a mussel-inspired bioreactor of elastic–mimetic cryogel and platelets

    Journal: Journal of Tissue Engineering

    doi: 10.1177/2041731418808633

    Growth factors release by the pDA/GC/Plt system. PDGF (a) and VEGF (b) were detected with ELISA. The release was prolonged in the pDA/GC/Plt group compared to that in the PRP group. A significant difference was observed after 3 h for both PDGF and VEGF. Chamber fluid was extracted and tested by ELISA for PDGF (c) and VEGF (d). pDA/GC/Plt incorporated into the TEC had significantly higher levels of PDGF and VEGF from days 7 and 3, respectively (p
    Figure Legend Snippet: Growth factors release by the pDA/GC/Plt system. PDGF (a) and VEGF (b) were detected with ELISA. The release was prolonged in the pDA/GC/Plt group compared to that in the PRP group. A significant difference was observed after 3 h for both PDGF and VEGF. Chamber fluid was extracted and tested by ELISA for PDGF (c) and VEGF (d). pDA/GC/Plt incorporated into the TEC had significantly higher levels of PDGF and VEGF from days 7 and 3, respectively (p

    Techniques Used: Enzyme-linked Immunosorbent Assay

    4) Product Images from "Tumor cell-macrophage interactions increase angiogenesis through secretion of EMMPRIN"

    Article Title: Tumor cell-macrophage interactions increase angiogenesis through secretion of EMMPRIN

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2013.00178

    EMMPRIN neutralization inhibits secretion of VEGF and MMP-9 . 5 × 10 5 A498 or MCF-7 cells were incubated separately or in co-cultures with 2.5 × 10 5 U937 cells in a serum-free medium supplemented with TNFα (1 ng/ml) for 48 h, with or without the addition of anti-EMMPRIN (2 ng/ml). Concentrations of (A) MMP-9 and (B) VEGF were determined in the supernatants using ELISA ( n = 7).
    Figure Legend Snippet: EMMPRIN neutralization inhibits secretion of VEGF and MMP-9 . 5 × 10 5 A498 or MCF-7 cells were incubated separately or in co-cultures with 2.5 × 10 5 U937 cells in a serum-free medium supplemented with TNFα (1 ng/ml) for 48 h, with or without the addition of anti-EMMPRIN (2 ng/ml). Concentrations of (A) MMP-9 and (B) VEGF were determined in the supernatants using ELISA ( n = 7).

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

    Effect of monocyte supernatants on cancer cell expression of VEGF and MMP-9 . 2 × 10 5 A498 or MCF-7 cells were separately incubated in the presence of TNFα (1 ng/ml) for 48 h with or without the addition of diluted (1:4) supernatants derived from U937 cells, and with the neutralizing anti-EMMPRIN antibody (2 ng/ml). Concentrations of (A) MMP-9 and (B) VEGF were determined by ELISA ( n = 5).
    Figure Legend Snippet: Effect of monocyte supernatants on cancer cell expression of VEGF and MMP-9 . 2 × 10 5 A498 or MCF-7 cells were separately incubated in the presence of TNFα (1 ng/ml) for 48 h with or without the addition of diluted (1:4) supernatants derived from U937 cells, and with the neutralizing anti-EMMPRIN antibody (2 ng/ml). Concentrations of (A) MMP-9 and (B) VEGF were determined by ELISA ( n = 5).

    Techniques Used: Expressing, Incubation, Derivative Assay, Enzyme-linked Immunosorbent Assay

    Effect of cancer cell supernatants on monocyte expression of VEGF and MMP-9 is mediated through soluble EMMPRIN . 2 × 10 5 U937 cells were separately incubated in the presence of TNFα (1 ng/ml) for 48 h with or without the addition of diluted (1:4) supernatants derived from A498 or MCF-7 cells, and with the neutralizing anti-EMMPRIN antibody (2 ng/ml). Concentrations of (A) MMP-9 and (B) VEGF were determined by ELISA ( n = 5).
    Figure Legend Snippet: Effect of cancer cell supernatants on monocyte expression of VEGF and MMP-9 is mediated through soluble EMMPRIN . 2 × 10 5 U937 cells were separately incubated in the presence of TNFα (1 ng/ml) for 48 h with or without the addition of diluted (1:4) supernatants derived from A498 or MCF-7 cells, and with the neutralizing anti-EMMPRIN antibody (2 ng/ml). Concentrations of (A) MMP-9 and (B) VEGF were determined by ELISA ( n = 5).

    Techniques Used: Expressing, Incubation, Derivative Assay, Enzyme-linked Immunosorbent Assay

    Cell–cell contact is not required for induction of MMP-9 and VEGF . 2 × 10 5 A498 or MCF-7 cells or 1 × 10 5 U937 cells were incubated with TNFα (1 ng/ml) for 48 h, separately, in a mixed co-culture where cell–cell contact was allowed, or in inserts with a small pore size (0.3 μm) that precluded cell migration and cell–cell contact. Concentrations of (A) MMP-9 and (B) VEGF were determined by ELISA ( n = 8).
    Figure Legend Snippet: Cell–cell contact is not required for induction of MMP-9 and VEGF . 2 × 10 5 A498 or MCF-7 cells or 1 × 10 5 U937 cells were incubated with TNFα (1 ng/ml) for 48 h, separately, in a mixed co-culture where cell–cell contact was allowed, or in inserts with a small pore size (0.3 μm) that precluded cell migration and cell–cell contact. Concentrations of (A) MMP-9 and (B) VEGF were determined by ELISA ( n = 8).

    Techniques Used: Incubation, Co-Culture Assay, Migration, Enzyme-linked Immunosorbent Assay

    Effect of recombinant EMMPRIN on the secretion of MMP-9, VEGF, and EMMPRIN . 5 × 10 5 A498, MCF-7 or U937 cells were incubated separately in a serum-free medium with or without TNFα (1 ng/ml) for 48 h, and with the addition of increasing amounts of recombinant EMMPRIN or the IgG Fc fragment (at 200 ng/ml). Concentrations of MMP-9 and VEGF were determined in the supernatants using ELISA ( n = 7).
    Figure Legend Snippet: Effect of recombinant EMMPRIN on the secretion of MMP-9, VEGF, and EMMPRIN . 5 × 10 5 A498, MCF-7 or U937 cells were incubated separately in a serum-free medium with or without TNFα (1 ng/ml) for 48 h, and with the addition of increasing amounts of recombinant EMMPRIN or the IgG Fc fragment (at 200 ng/ml). Concentrations of MMP-9 and VEGF were determined in the supernatants using ELISA ( n = 7).

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

    Effect of EMMPRIN siRNA on the secretion of MMP-9, VEGF and EMMPRIN . 0.6 × 10 5 A498 or MCF-7 cells were incubated separately or in co-cultures with 0.3 × 10 6 U937 cells in a serum-free medium supplemented with TNFα (1 ng/ml) for 48 h. Tumor cells were first transfected with 5 nM of each of the two different EMMPRIN siRNA molecules, their combination or the negative control (NC), or left untreated. Concentrations of (A) MMP-9, (B) VEGF, and (C) EMMPRIN were determined in the supernatants using ELISA ( n = 5).
    Figure Legend Snippet: Effect of EMMPRIN siRNA on the secretion of MMP-9, VEGF and EMMPRIN . 0.6 × 10 5 A498 or MCF-7 cells were incubated separately or in co-cultures with 0.3 × 10 6 U937 cells in a serum-free medium supplemented with TNFα (1 ng/ml) for 48 h. Tumor cells were first transfected with 5 nM of each of the two different EMMPRIN siRNA molecules, their combination or the negative control (NC), or left untreated. Concentrations of (A) MMP-9, (B) VEGF, and (C) EMMPRIN were determined in the supernatants using ELISA ( n = 5).

    Techniques Used: Incubation, Transfection, Negative Control, Enzyme-linked Immunosorbent Assay

    The effect of co-culture on the secretion of EMMPRIN, MMP-9 and VEGF . 10 6 A498 or MCF-7 cells were incubated in a serum-free medium either separately or with 0.5 × 10 6 U937 cells in co-culture for 48 h, with or without the addition of TNFα (1 ng/ml), and 0.5 × 10 6 U937 cells were incubated in a serum-free medium with or without the addition of TNFα (1 ng/ml). (A) Representative dot plot for the A498 and U937 co-cultures. Light blue and orange histograms—EMMPRIN expression in single cultures of A498 cells and U937 cells, respectively; Blue and red histograms—EMMPRIN expression measured separately on A498 or U937 cells, respectively, incubated in their co-cultures. Gray histogram—isotype control. (B) Mean fluorescence (MF) of the membranal expression of EMMPRIN that was evaluated by flow cytometry ( n = 8). Concentrations of secreted proteins were determined in the supernatants by ELISA for (C) EMMPRIN ( n = 6), (D) MMP-9 ( n = 8) and (E) VEGF ( n = 8).
    Figure Legend Snippet: The effect of co-culture on the secretion of EMMPRIN, MMP-9 and VEGF . 10 6 A498 or MCF-7 cells were incubated in a serum-free medium either separately or with 0.5 × 10 6 U937 cells in co-culture for 48 h, with or without the addition of TNFα (1 ng/ml), and 0.5 × 10 6 U937 cells were incubated in a serum-free medium with or without the addition of TNFα (1 ng/ml). (A) Representative dot plot for the A498 and U937 co-cultures. Light blue and orange histograms—EMMPRIN expression in single cultures of A498 cells and U937 cells, respectively; Blue and red histograms—EMMPRIN expression measured separately on A498 or U937 cells, respectively, incubated in their co-cultures. Gray histogram—isotype control. (B) Mean fluorescence (MF) of the membranal expression of EMMPRIN that was evaluated by flow cytometry ( n = 8). Concentrations of secreted proteins were determined in the supernatants by ELISA for (C) EMMPRIN ( n = 6), (D) MMP-9 ( n = 8) and (E) VEGF ( n = 8).

    Techniques Used: Co-Culture Assay, Incubation, Expressing, Fluorescence, Flow Cytometry, Cytometry, Enzyme-linked Immunosorbent Assay

    5) Product Images from "Lipopolysaccharide preconditioning enhances the efficacy of mesenchymal stem cells transplantation in a rat model of acute myocardial infarction"

    Article Title: Lipopolysaccharide preconditioning enhances the efficacy of mesenchymal stem cells transplantation in a rat model of acute myocardial infarction

    Journal: Journal of Biomedical Science

    doi: 10.1186/1423-0127-16-74

    VEGF concentration in the culture supernant of MSCs . ELISA analysis of supernatant after stimulation of LPS is shown. Wild MSCs were exposed to increasing doses of LPS for 48 hours. VEGF concentration increased after LPS treatment and VEGF concentration was the highest after incubation with 1.0 μg/ml LPS. B. In the presence of NF-κB inhibitor-PDTC, LPS stimulation caused a subsequent decrease in VEGF expression compared with that without NF-κB inhibition. LPS stimulation on tMSCs caused an obvious decrease in VEGF expression compared with that of wild MSCs. (a. VEGF concentration of wMSCs without stimulation of LPS; b. VEGF concentration of wMSCs with 1.0 μg/ml LPS stimulation; c. VEGF concentration of wMSCs with stimulation of 1.0 μg/ml LPS and 5 nmol/L PDTC; d. VEGF concentration of TLR4 gene deleted MSCs with stimulation of 1.0 μg/ml LPS) Data are mean ± SEM. * P
    Figure Legend Snippet: VEGF concentration in the culture supernant of MSCs . ELISA analysis of supernatant after stimulation of LPS is shown. Wild MSCs were exposed to increasing doses of LPS for 48 hours. VEGF concentration increased after LPS treatment and VEGF concentration was the highest after incubation with 1.0 μg/ml LPS. B. In the presence of NF-κB inhibitor-PDTC, LPS stimulation caused a subsequent decrease in VEGF expression compared with that without NF-κB inhibition. LPS stimulation on tMSCs caused an obvious decrease in VEGF expression compared with that of wild MSCs. (a. VEGF concentration of wMSCs without stimulation of LPS; b. VEGF concentration of wMSCs with 1.0 μg/ml LPS stimulation; c. VEGF concentration of wMSCs with stimulation of 1.0 μg/ml LPS and 5 nmol/L PDTC; d. VEGF concentration of TLR4 gene deleted MSCs with stimulation of 1.0 μg/ml LPS) Data are mean ± SEM. * P

    Techniques Used: Concentration Assay, Enzyme-linked Immunosorbent Assay, Incubation, Expressing, Inhibition

    6) Product Images from "Interleukin-6 Receptor-Mediated Activation of Signal Transducer and Activator of Transcription-3 (STAT3) Promotes Choroidal Neovascularization"

    Article Title: Interleukin-6 Receptor-Mediated Activation of Signal Transducer and Activator of Transcription-3 (STAT3) Promotes Choroidal Neovascularization

    Journal: The American Journal of Pathology

    doi: 10.2353/ajpath.2007.061018

    In vivo effects of IL-6R blockade on choroidal expression of inflammatory and angiogenic molecules analyzed by RT-PCR ( A ) and ELISA ( B–D ). IL-6R blockade by the administration of MR16-1 significantly suppressed protein levels of ICAM-1 ( B ), MCP-1 ( C ), and VEGF ( D ). n = 8 to 10. * P
    Figure Legend Snippet: In vivo effects of IL-6R blockade on choroidal expression of inflammatory and angiogenic molecules analyzed by RT-PCR ( A ) and ELISA ( B–D ). IL-6R blockade by the administration of MR16-1 significantly suppressed protein levels of ICAM-1 ( B ), MCP-1 ( C ), and VEGF ( D ). n = 8 to 10. * P

    Techniques Used: In Vivo, Expressing, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    7) Product Images from "Inhibition of APN/CD13 leads to suppressed progressive potential in ovarian carcinoma cells"

    Article Title: Inhibition of APN/CD13 leads to suppressed progressive potential in ovarian carcinoma cells

    Journal: BMC Cancer

    doi: 10.1186/1471-2407-7-140

    Decrease of MMP-2 and VEGF expression caused by RNA interference of APN/CD13 in ES-2 cells using MMP-2 and VEGF ELISA kit. The MMP-2 and VEGD expression in the conditioned medium of si-CD13-transfected ES-2 cells was significantly lower than that of si-cont-transfected cells. Data are expressed as the mean ± SD, A; * p
    Figure Legend Snippet: Decrease of MMP-2 and VEGF expression caused by RNA interference of APN/CD13 in ES-2 cells using MMP-2 and VEGF ELISA kit. The MMP-2 and VEGD expression in the conditioned medium of si-CD13-transfected ES-2 cells was significantly lower than that of si-cont-transfected cells. Data are expressed as the mean ± SD, A; * p

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

    8) Product Images from "Methodological differences account for inconsistencies in reported free VEGF concentrations in pregnant rats"

    Article Title: Methodological differences account for inconsistencies in reported free VEGF concentrations in pregnant rats

    Journal: American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

    doi: 10.1152/ajpregu.00544.2013

    Plasma vascular endothelial growth factor (VEGF) in nonpregnant and pregnant rats measured by the rat ELISA. Circles show values for individual rats. Lines show the group median (0 pg/ml for day 19 pregnant rats). Significant difference from: nonpregnant,
    Figure Legend Snippet: Plasma vascular endothelial growth factor (VEGF) in nonpregnant and pregnant rats measured by the rat ELISA. Circles show values for individual rats. Lines show the group median (0 pg/ml for day 19 pregnant rats). Significant difference from: nonpregnant,

    Techniques Used: Enzyme-linked Immunosorbent Assay

    9) Product Images from "Vascular endothelial growth factor/vascular permeability factor is an autocrine growth factor for AIDS-Kaposi sarcoma"

    Article Title: Vascular endothelial growth factor/vascular permeability factor is an autocrine growth factor for AIDS-Kaposi sarcoma

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

    doi:

    Expression of VEGF mRNA in several AIDS–KS cells lines. ( A ) Total RNA (15 μg) from KSC10, KSC29, KSC13, KSC59, and KSY1 were electrophoresed, blotted, and hybridized to the human VEGF cDNA and β-actin probe. ( B ) Total RNA (15 μg) was isolated from KSC10, HUVEC, and AoSM and analyzed as in A . ( C ) Supernatants from equal numbers of cells from KSY1, KSC10, AoSM, HUVEC, and T1 were collected after 48 hr and analyzed for VEGF protein by ELISA.
    Figure Legend Snippet: Expression of VEGF mRNA in several AIDS–KS cells lines. ( A ) Total RNA (15 μg) from KSC10, KSC29, KSC13, KSC59, and KSY1 were electrophoresed, blotted, and hybridized to the human VEGF cDNA and β-actin probe. ( B ) Total RNA (15 μg) was isolated from KSC10, HUVEC, and AoSM and analyzed as in A . ( C ) Supernatants from equal numbers of cells from KSY1, KSC10, AoSM, HUVEC, and T1 were collected after 48 hr and analyzed for VEGF protein by ELISA.

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

    Effect of VEGF antisense (AS-1 and AS-3) and scramble (S) oligonucleotides on VEGF expression. Total RNA was isolated from AIDS–KS cells treated with various concentrations of AS-1 ( A ), AS-3 ( B ), and S ( C ). Total RNA was reverse transcribed to generate cDNA. PCR was carried out for VEGF and β-actin. ( Upper ) PCR products of 535 bp and 403 bp corresponding to VEGF 121 and VEGF 165 mRNA species of VEGF. ( Lower ) The 548-bp PCR product of β-actin. (NT, no treatment; M, molecular size marker.) The numbers 25-41 and 18-33 represent PCR cycles. ( D ) The supernatants of KS cells treated with AS-3 and scrambled VEGF antisense oligonucleotide were also collected at 48 hr, and VEGF protein was quantitated by ELISA. The results represent the mean ± SD of two separate experiments done in duplicate.
    Figure Legend Snippet: Effect of VEGF antisense (AS-1 and AS-3) and scramble (S) oligonucleotides on VEGF expression. Total RNA was isolated from AIDS–KS cells treated with various concentrations of AS-1 ( A ), AS-3 ( B ), and S ( C ). Total RNA was reverse transcribed to generate cDNA. PCR was carried out for VEGF and β-actin. ( Upper ) PCR products of 535 bp and 403 bp corresponding to VEGF 121 and VEGF 165 mRNA species of VEGF. ( Lower ) The 548-bp PCR product of β-actin. (NT, no treatment; M, molecular size marker.) The numbers 25-41 and 18-33 represent PCR cycles. ( D ) The supernatants of KS cells treated with AS-3 and scrambled VEGF antisense oligonucleotide were also collected at 48 hr, and VEGF protein was quantitated by ELISA. The results represent the mean ± SD of two separate experiments done in duplicate.

    Techniques Used: Expressing, Isolation, Polymerase Chain Reaction, Marker, Enzyme-linked Immunosorbent Assay

    10) Product Images from "Large adipose tissue generation in a mussel-inspired bioreactor of elastic–mimetic cryogel and platelets"

    Article Title: Large adipose tissue generation in a mussel-inspired bioreactor of elastic–mimetic cryogel and platelets

    Journal: Journal of Tissue Engineering

    doi: 10.1177/2041731418808633

    Growth factors release by the pDA/GC/Plt system. PDGF (a) and VEGF (b) were detected with ELISA. The release was prolonged in the pDA/GC/Plt group compared to that in the PRP group. A significant difference was observed after 3 h for both PDGF and VEGF. Chamber fluid was extracted and tested by ELISA for PDGF (c) and VEGF (d). pDA/GC/Plt incorporated into the TEC had significantly higher levels of PDGF and VEGF from days 7 and 3, respectively (p
    Figure Legend Snippet: Growth factors release by the pDA/GC/Plt system. PDGF (a) and VEGF (b) were detected with ELISA. The release was prolonged in the pDA/GC/Plt group compared to that in the PRP group. A significant difference was observed after 3 h for both PDGF and VEGF. Chamber fluid was extracted and tested by ELISA for PDGF (c) and VEGF (d). pDA/GC/Plt incorporated into the TEC had significantly higher levels of PDGF and VEGF from days 7 and 3, respectively (p

    Techniques Used: Enzyme-linked Immunosorbent Assay

    11) Product Images from "Role of endoplasmic reticulum stress in 12/15-lipoxygenase-induced retinal microvascular dysfunction in a mouse model of diabetic retinopathy"

    Article Title: Role of endoplasmic reticulum stress in 12/15-lipoxygenase-induced retinal microvascular dysfunction in a mouse model of diabetic retinopathy

    Journal: Diabetologia

    doi: 10.1007/s00125-018-4560-z

    ER stress inhibition attenuates 15-HETE-induced VEGFR2 phosphorylation. ( a ) ELISA of VEGF levels in supernatant of HRECs treated with vehicle or 15-HETE for 24 h showing no significant difference in the VEGF levels. Data represent individual data points with means ± SEM. ( b ) Immunoprecipitation (IP) of VEGFR2 in HRECs treated with 15-HETE in the presence or absence of PBA or apocynin for 5 min, followed by immunoblotting (IB) of phosphotyrosine (pTyr). Normalisation was done by re-blotting the membrane for VEGFR2. ( c ) Densitometry analysis shows a significant increase in VEGFR2 phosphorylation by 15-HETE compared with the control. ER stress inhibitor (PBA) and NADPH oxidase inhibitor (apocynin) reduced the effect of 15-HETE on VEGFR2 phosphorylation. Data represent individual data points with means ± SEM; * p
    Figure Legend Snippet: ER stress inhibition attenuates 15-HETE-induced VEGFR2 phosphorylation. ( a ) ELISA of VEGF levels in supernatant of HRECs treated with vehicle or 15-HETE for 24 h showing no significant difference in the VEGF levels. Data represent individual data points with means ± SEM. ( b ) Immunoprecipitation (IP) of VEGFR2 in HRECs treated with 15-HETE in the presence or absence of PBA or apocynin for 5 min, followed by immunoblotting (IB) of phosphotyrosine (pTyr). Normalisation was done by re-blotting the membrane for VEGFR2. ( c ) Densitometry analysis shows a significant increase in VEGFR2 phosphorylation by 15-HETE compared with the control. ER stress inhibitor (PBA) and NADPH oxidase inhibitor (apocynin) reduced the effect of 15-HETE on VEGFR2 phosphorylation. Data represent individual data points with means ± SEM; * p

    Techniques Used: Inhibition, Enzyme-linked Immunosorbent Assay, Immunoprecipitation

    12) Product Images from "Chitosan-Alginate Scaffold Culture System for Hepatocellular Carcinoma Increases Malignancy and Drug Resistance"

    Article Title: Chitosan-Alginate Scaffold Culture System for Hepatocellular Carcinoma Increases Malignancy and Drug Resistance

    Journal: Pharmaceutical research

    doi: 10.1007/s11095-010-0198-3

    Comparison of growth factor expression profiles of hepatocellular carcinoma cells cultured in vitro for 10 days on different culture conditions. (a) IL-8, (b) bFGF, and (c) VEGF secretion by PCL and HepG2 cells cultured on 2D tissue culture plates, Matrigel matrices, and CA scaffolds as determined by ELISA. Results are mean ± s.d., and * indicates at least one of the means in that group is statistically different from the others, p
    Figure Legend Snippet: Comparison of growth factor expression profiles of hepatocellular carcinoma cells cultured in vitro for 10 days on different culture conditions. (a) IL-8, (b) bFGF, and (c) VEGF secretion by PCL and HepG2 cells cultured on 2D tissue culture plates, Matrigel matrices, and CA scaffolds as determined by ELISA. Results are mean ± s.d., and * indicates at least one of the means in that group is statistically different from the others, p

    Techniques Used: Expressing, Cell Culture, In Vitro, Enzyme-linked Immunosorbent Assay

    13) Product Images from "A Pilot Study Evaluating Combinatorial and Simultaneous Delivery of Polyethylenimine-Plasmid DNA Complexes Encoding for VEGF and PDGF for Bone Regeneration in Calvarial Bone Defects"

    Article Title: A Pilot Study Evaluating Combinatorial and Simultaneous Delivery of Polyethylenimine-Plasmid DNA Complexes Encoding for VEGF and PDGF for Bone Regeneration in Calvarial Bone Defects

    Journal: Current pharmaceutical biotechnology

    doi:

    Detection of PDGF-BB and VEGF proteins in cell supernatants by ELISA after BMSC transfection with PEI-pPDGF-B and PEI-pVEGF complexes, respectively (n = 3, ***p
    Figure Legend Snippet: Detection of PDGF-BB and VEGF proteins in cell supernatants by ELISA after BMSC transfection with PEI-pPDGF-B and PEI-pVEGF complexes, respectively (n = 3, ***p

    Techniques Used: Enzyme-linked Immunosorbent Assay, Transfection

    14) Product Images from "Leptin pro-angiogenic signature in breast cancer is linked to IL-1 signalling"

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

    Journal: British Journal of Cancer

    doi: 10.1038/sj.bjc.6606013

    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
    Figure Legend 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

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

    15) Product Images from "Large adipose tissue generation in a mussel-inspired bioreactor of elastic–mimetic cryogel and platelets"

    Article Title: Large adipose tissue generation in a mussel-inspired bioreactor of elastic–mimetic cryogel and platelets

    Journal: Journal of Tissue Engineering

    doi: 10.1177/2041731418808633

    Growth factors release by the pDA/GC/Plt system. PDGF (a) and VEGF (b) were detected with ELISA. The release was prolonged in the pDA/GC/Plt group compared to that in the PRP group. A significant difference was observed after 3 h for both PDGF and VEGF. Chamber fluid was extracted and tested by ELISA for PDGF (c) and VEGF (d). pDA/GC/Plt incorporated into the TEC had significantly higher levels of PDGF and VEGF from days 7 and 3, respectively (p
    Figure Legend Snippet: Growth factors release by the pDA/GC/Plt system. PDGF (a) and VEGF (b) were detected with ELISA. The release was prolonged in the pDA/GC/Plt group compared to that in the PRP group. A significant difference was observed after 3 h for both PDGF and VEGF. Chamber fluid was extracted and tested by ELISA for PDGF (c) and VEGF (d). pDA/GC/Plt incorporated into the TEC had significantly higher levels of PDGF and VEGF from days 7 and 3, respectively (p

    Techniques Used: Enzyme-linked Immunosorbent Assay

    16) Product Images from "Augmentation of neovascularization in murine hindlimb ischemia by combined therapy with simvastatin and bone marrow-derived mesenchymal stem cells transplantation"

    Article Title: Augmentation of neovascularization in murine hindlimb ischemia by combined therapy with simvastatin and bone marrow-derived mesenchymal stem cells transplantation

    Journal: Journal of Biomedical Science

    doi: 10.1186/1423-0127-17-75

    Effect of simvastatin on the release of VEGF by bone marrow-derived MSCs in vitro . MSCs were exposed to increasing doses of simvastatin for 24 h. Then, 24 h after replacement of the culture medium, VEGF concentration was measured by ELISA. Means ± SD of measurements from one experiment (n = 4). * p
    Figure Legend Snippet: Effect of simvastatin on the release of VEGF by bone marrow-derived MSCs in vitro . MSCs were exposed to increasing doses of simvastatin for 24 h. Then, 24 h after replacement of the culture medium, VEGF concentration was measured by ELISA. Means ± SD of measurements from one experiment (n = 4). * p

    Techniques Used: Derivative Assay, In Vitro, Concentration Assay, Enzyme-linked Immunosorbent Assay

    17) Product Images from "Viral G protein-coupled receptor up-regulates Angiopoietin-like 4 promoting angiogenesis and vascular permeability in Kaposi's sarcoma"

    Article Title: Viral G protein-coupled receptor up-regulates Angiopoietin-like 4 promoting angiogenesis and vascular permeability in Kaposi's sarcoma

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

    doi: 10.1073/pnas.1001065107

    VEGF is not sufficient for the increased vessel permeability in vGPCR tumorigenesis. Human KS ( A ) and murine vGPCR ( B ) tumors are composed of malignant spindle cells and irregular vascular channels lined by atypical endothelium. The atypically lined vessels, containing red and white blood cells, are clearly shown in the insets (arrowheads); the arrows point to a mitotic figure. In both cases part of the remaining squamous epidermis can be seen in the top right area. Both human ( C ) and vGPCR (experimental) ( D ) KS are characterized by increased vascular permeability. This is evident in the pictures, where the proliferating cells are separated by edematous, lightly stained areas (arrows). ( E ) A series of normal vascular structures in the normal dermis. Note the distinctively normal, regular features of the blood vessels, especially of the endothelium (arrows). The endothelial lining is better observed at a higher magnification ( Inset , arrow); the cells are uniformly flat with a spindle-shaped typical nuclei. ( F ) of HMVEC transfected with pCEFL GFP (Control), pCEFL Tet REV TA (rtTA), pBIG AU5 vGPCR (vGPCR), or pCEFL AU5 vGPCR (AU5 vGPCR). Cells were treated with (1 μg/mL) doxycycline (Dox) for 24 h. ( G ) FITC–dextran permeability was determined in mature HMVEC monolayers transfected with pCEFL Tet REV TA (rtTA) and pBIG AU5 vGPCR (vGPCR) and treated with (1 μg/mL) Dox for 24 h. hVEGF (50 ng/mL; 30 min) was used as a control. ( H ) HMVECs were transfected with pCEFL Tet REV TA (rtTA) and pBIG AU5 vGPCR (vGPCR). Cells were treated with (1 μg/mL) Dox for 24 h, and the levels of VEGF were determined by ELISA. ( I ) FITC–dextran permeability was determined in mature HMVEC monolayers transfected with VEGF, Scrambled, or no siRNA and then with pCEFL Tet REV TA (rtTA) and pBIG AU5 vGPCR (vGPCR), and treated with (1 μg/mL) Dox for 24 h. ( J ) FITC–dextran permeability was determined in mature HMVEC monolayers transfected with pCEFL Tet REV TA (rtTA) and pBIG AU5 vGPCR (vGPCR), and treated with (1 μg/mL) Dox for 24 h and with su1498 for 45 min. hVEGF (50 ng/mL; 30 min) served as a control ( I–J ).
    Figure Legend Snippet: VEGF is not sufficient for the increased vessel permeability in vGPCR tumorigenesis. Human KS ( A ) and murine vGPCR ( B ) tumors are composed of malignant spindle cells and irregular vascular channels lined by atypical endothelium. The atypically lined vessels, containing red and white blood cells, are clearly shown in the insets (arrowheads); the arrows point to a mitotic figure. In both cases part of the remaining squamous epidermis can be seen in the top right area. Both human ( C ) and vGPCR (experimental) ( D ) KS are characterized by increased vascular permeability. This is evident in the pictures, where the proliferating cells are separated by edematous, lightly stained areas (arrows). ( E ) A series of normal vascular structures in the normal dermis. Note the distinctively normal, regular features of the blood vessels, especially of the endothelium (arrows). The endothelial lining is better observed at a higher magnification ( Inset , arrow); the cells are uniformly flat with a spindle-shaped typical nuclei. ( F ) of HMVEC transfected with pCEFL GFP (Control), pCEFL Tet REV TA (rtTA), pBIG AU5 vGPCR (vGPCR), or pCEFL AU5 vGPCR (AU5 vGPCR). Cells were treated with (1 μg/mL) doxycycline (Dox) for 24 h. ( G ) FITC–dextran permeability was determined in mature HMVEC monolayers transfected with pCEFL Tet REV TA (rtTA) and pBIG AU5 vGPCR (vGPCR) and treated with (1 μg/mL) Dox for 24 h. hVEGF (50 ng/mL; 30 min) was used as a control. ( H ) HMVECs were transfected with pCEFL Tet REV TA (rtTA) and pBIG AU5 vGPCR (vGPCR). Cells were treated with (1 μg/mL) Dox for 24 h, and the levels of VEGF were determined by ELISA. ( I ) FITC–dextran permeability was determined in mature HMVEC monolayers transfected with VEGF, Scrambled, or no siRNA and then with pCEFL Tet REV TA (rtTA) and pBIG AU5 vGPCR (vGPCR), and treated with (1 μg/mL) Dox for 24 h. ( J ) FITC–dextran permeability was determined in mature HMVEC monolayers transfected with pCEFL Tet REV TA (rtTA) and pBIG AU5 vGPCR (vGPCR), and treated with (1 μg/mL) Dox for 24 h and with su1498 for 45 min. hVEGF (50 ng/mL; 30 min) served as a control ( I–J ).

    Techniques Used: Permeability, Staining, Transfection, Enzyme-linked Immunosorbent Assay

    18) Product Images from "Farnesoid X receptor, overexpressed in pancreatic cancer with lymph node metastasis promotes cell migration and invasion"

    Article Title: Farnesoid X receptor, overexpressed in pancreatic cancer with lymph node metastasis promotes cell migration and invasion

    Journal: British Journal of Cancer

    doi: 10.1038/bjc.2011.37

    Effects of FXR siRNA on NF- κ B p65 and VEGF activities. CS, control siRNA; FS, FXR siRNA. ( A ) Nuclear extracts were prepared from control siRNA or FXR siRNA-transfected MIA PaCa2 and PANC-1 cells and subjected to analysis for NF- κ B p65 activity as measured by Active Motif enzyme-linked immunosorbent assay (ELISA). ( B ) The culture medium of control siRNA or FXR siRNA-transfected MIA-PaCa2 and PANC-1 cells was used for the detection of VEGF using ELISA, as described under Materials and Methods. The relative-fold change of NF- κ B p65 or VEGF activity in FXR siRNA-transfected cells was normalised against control FXR siRNA-transfected cells. Values in control siRNA-transfected cells were arbitrarily set to 1. Columns, mean of three independent experiments; bars, s.e.m. * P
    Figure Legend Snippet: Effects of FXR siRNA on NF- κ B p65 and VEGF activities. CS, control siRNA; FS, FXR siRNA. ( A ) Nuclear extracts were prepared from control siRNA or FXR siRNA-transfected MIA PaCa2 and PANC-1 cells and subjected to analysis for NF- κ B p65 activity as measured by Active Motif enzyme-linked immunosorbent assay (ELISA). ( B ) The culture medium of control siRNA or FXR siRNA-transfected MIA-PaCa2 and PANC-1 cells was used for the detection of VEGF using ELISA, as described under Materials and Methods. The relative-fold change of NF- κ B p65 or VEGF activity in FXR siRNA-transfected cells was normalised against control FXR siRNA-transfected cells. Values in control siRNA-transfected cells were arbitrarily set to 1. Columns, mean of three independent experiments; bars, s.e.m. * P

    Techniques Used: Transfection, Activity Assay, Enzyme-linked Immunosorbent Assay

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    Immunostaining:

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    Article Snippet: .. Immunostaining and immunocytofluorescence were performed using the following antibodies: rat anti–Vegfr3 (eBioscience), rat anti–PECAM-1 (BD), rabbit anti-Lyve1 (Abcam), monoclonal anti-VEGFD (R & D Systems), and rabbit anti-IGF1 (Santa Cruz Biotechnology, Inc.). .. Nonfluorescent antibodies were visualized after mounting slides in Cytoseal (Thermo Fisher Scientific).

    Enzyme-linked Immunosorbent Assay:

    Article Title: A Virus-Derived Immune Modulating Serpin Accelerates Wound Closure with Improved Collagen Remodeling
    Article Snippet: Enzyme-Linked Immunosorbent Assay (ELISA) Wound beds and surrounding tissue (same total size) were collected on days 1, 4 and 7 post-wounding and homogenized with a blade homogenizer into 400 µL RIPA buffer containing 1× protease inhibitor cocktail (Bimake, Houston, TX, USA, #B14001) on ice. .. Vascular endothelial growth factor (VEGF) was quantified with the Mouse VEGF DuoSet ELISA (R & D Systems, Minneapolis, MN, USA, #DY493) and DuoSet ELISA Ancillary Reagent Kit 2 (R & D Systems, Minneapolis, MN, USA, #DY008) according to manufacturer’s instructions. .. Quantified VEGF was normalized to total protein using the BCA assay (ThermoFisher Scientific, Waltham, MA, USA, #23225).

    Article Title: Acute Exposure to Low Level Light at Night is Sufficient to Induce Neurological Changes and Depressive-like Behavior
    Article Snippet: Next, a Pierce BCA Protein Assay (Thermo Fisher Scientific, Waltham, MA) was performed according to the manufacturer’s instructions to determine the protein concentration in each sample and to ensure for equal amounts of protein load during the subsequent ELISA. .. To determine the concentration of VEGF-A in each hippocampus (350μg of protein), a mouse VEGF ELISA (MMV00, R & D Systems, Minneapolis, MN) was performed according to the manufacturer’s instructions (assay range 7.8–500 pg/ml); samples were run in duplicate. .. The plates were read using a SPECTRAmax Plus plate reader (Molecular Devices, San Jose, CA).

    Article Title: Effects of ginseng saponins isolated from Red Ginseng roots on burn wound healing in mice
    Article Snippet: Collagen (Type I)-coated six-well plates were purchased from Sumitomo Bakelite (Tokyo, Japan). .. Human and mouse VEGF ELISA kits and mouse IL-1 β were obtained from R & D Systems Inc. (Minneapolis, MN, U.S.A.). .. Rat monoclonal anti-mouse Ki-67 antibody and rabbit polyclonal anti-rat biotin-labeled immunoglobulin antibody peroxidase-labeled streptavidin were purchased from DakoCytomation (Kyoto, Japan).

    Article Title: KSHV G-protein coupled receptor vGPCR oncogenic signaling upregulation of Cyclooxygenase-2 expression mediates angiogenesis and tumorigenesis in Kaposi’s sarcoma
    Article Snippet: VEGF production testTumor samples were weighted and homogenized in buffer TBS 0.1% BSA with the addition of a protease inhibitor cocktail (Sigma, Saint Louis, Missouri) in a volume proportional to their weight. .. Cell supernatants were assayed after centrifugation at 2,000 x g RT for 5 min. ELISA with anti-mouse-VEGF (R & D Systems, Minneapolis, Minnesota) was performed following the manufacturer’s instructions. .. VEGF levels from tumor samples were normalized based on lysate protein concentration.

    Concentration Assay:

    Article Title: Acute Exposure to Low Level Light at Night is Sufficient to Induce Neurological Changes and Depressive-like Behavior
    Article Snippet: Next, a Pierce BCA Protein Assay (Thermo Fisher Scientific, Waltham, MA) was performed according to the manufacturer’s instructions to determine the protein concentration in each sample and to ensure for equal amounts of protein load during the subsequent ELISA. .. To determine the concentration of VEGF-A in each hippocampus (350μg of protein), a mouse VEGF ELISA (MMV00, R & D Systems, Minneapolis, MN) was performed according to the manufacturer’s instructions (assay range 7.8–500 pg/ml); samples were run in duplicate. .. The plates were read using a SPECTRAmax Plus plate reader (Molecular Devices, San Jose, CA).

    Centrifugation:

    Article Title: KSHV G-protein coupled receptor vGPCR oncogenic signaling upregulation of Cyclooxygenase-2 expression mediates angiogenesis and tumorigenesis in Kaposi’s sarcoma
    Article Snippet: VEGF production testTumor samples were weighted and homogenized in buffer TBS 0.1% BSA with the addition of a protease inhibitor cocktail (Sigma, Saint Louis, Missouri) in a volume proportional to their weight. .. Cell supernatants were assayed after centrifugation at 2,000 x g RT for 5 min. ELISA with anti-mouse-VEGF (R & D Systems, Minneapolis, Minnesota) was performed following the manufacturer’s instructions. .. VEGF levels from tumor samples were normalized based on lysate protein concentration.

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    R&D Systems vegf c enzyme immunoassay kit
    bFGF promotes <t>VEGF-C</t> via downregulation of miR-381 ( A ) JJ012 cells were incubated with bFGF (0–30 ng/mL) for 24 h; miR-381 expression was examined by qPCR ( n = 6). ( B and C ) JJ012 cells were transfected with miRNA control or miR-381 mimic for 24 h and stimulated with bFGF (30 ng/mL) for 24 h. VEGF-C expression was examined by qPCR and ELISA ( n = 5–7). ( D and E ) Medium was collected as CM, then applied to LECs for 24 h; capillary-like structure formation and in vitro cell migration in LECs was examined by tube formation and the Transwell assay (Scar bar = 100 μm) ( n = 5–7). ( F ) Cells were pretreated for 30 min with AG-1296 or PP2 and stimulated with bFGF (30 ng/mL) for 24 h. miR-381 expression was examined by qPCR ( n = 5). ( G ) Schematic 3′UTR representation of the human VEGF-C containing miR-381 binding site. ( H ) JJ012 cells were transfected with the wt-VEGFC-3′UTR or mt-VEGFC-3′UTR plasmids for 24 h and stimulated with bFGF (30 ng/mL) for 24 h; relative luciferase/renilla activities were measured as described in the Methods section ( n = 5). ( I ) JJ012 cells were pretreated for 30 min with AG-1296 or PP2 and stimulated with bFGF for 24 h. wt-VEGFC-3′UTR relative luciferase/renilla activities were measured as described in the Methods section ( n = 5). Data are expressed as the mean ± SEM: * P
    Vegf C Enzyme Immunoassay Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cytochrome P450 1B1-deficient ( <t>Cyp1b1</t> −/− ) retinal astrocytes (ACs) express reduced levels of inflammatory mediators. A – C : expression levels of various inflammatory factors assessed by real-time quantitative (q)PCR analysis: bone morphogenetic protein-7 (BMP-7) ( A ); monocyte chemoattractant protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), and neuronal nitric oxide synthase (nNOS) ( B ); and IL-1β, IL-6, INF-γ, and TNF-α ( C ). D : <t>VEGF-A</t> amounts determined by ELISA in both conditioned medium (CM) and AC lysates (CML). E : expression levels of various VEGF-A isoforms determined by real-time qPCR. Please note a significant decrease in the levels of BMP-7 and MCP-1 (** P
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    <t>VEGF-A</t> was another downstream proangiogenic factor of caspase 3 A. <t>ELISA</t> showing that VEGF-A concentrations of CM collected from 10 Gy-irradiated U87 cells treated with caspase 3 inhibitor, Z-DEVD-FMK, was much lower than controls. B. p-eIF4E induction in response to irradiation was inhibited when caspase 3 was inactivated. C. Ki8751, a VEGFR2 inhibitor, significantly mitigated the proliferation-stimulating effect of dying U87 cells on HUVEC-Fluc. D. Left panel, quantification analysis showing that Ki8751 decreased HUVEC migration towards CM from irradiated U87 cells. Right panel, representative images of HUVEC migration with or without administration of Ki8751 towards CM from irradiated U87 cells. Scale bar: 250 μm. E. A schematic representation of mechanisms underlying post-irradiation angiogenesis elicited by dying glioma cells.
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    Metformin prevents the NGF induced VEGF expression and angiogenic properties of ovarian cells. Ovarian cells were treated with metformin 10 mM for 48 h and/or NGF 100 ng/mL or 150 ng/mL (A2780/HOSE cells and SKOV3 cells, respectively) for 24 h or the last 2 h, and then processed to detect VEGF expression. ( A , C , E ) Representative agarose gels with PCR products of different VEGF transcripts (VEGF 121, VEGF 165 and VEGF 189 amino acids) in ovarian cells. Semi-quantification of N = 4 or more independent experiments. ( B , D , F ) VEGF detection in the culture supernatants of ovarian cells by enzyme-linked <t>immunosorbent</t> assay <t>(ELISA).</t> N = 4 or more independent experiments induplicate. ( G , H ) Angiogenic score calculated as indicated in the methodology section with conditioned medium from A2780 or SKOV3 cells, respectively. Bar = 50 µm. N = 4 or more independent experiments (4–8 images were evaluated per experiment). * p
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    bFGF promotes VEGF-C via downregulation of miR-381 ( A ) JJ012 cells were incubated with bFGF (0–30 ng/mL) for 24 h; miR-381 expression was examined by qPCR ( n = 6). ( B and C ) JJ012 cells were transfected with miRNA control or miR-381 mimic for 24 h and stimulated with bFGF (30 ng/mL) for 24 h. VEGF-C expression was examined by qPCR and ELISA ( n = 5–7). ( D and E ) Medium was collected as CM, then applied to LECs for 24 h; capillary-like structure formation and in vitro cell migration in LECs was examined by tube formation and the Transwell assay (Scar bar = 100 μm) ( n = 5–7). ( F ) Cells were pretreated for 30 min with AG-1296 or PP2 and stimulated with bFGF (30 ng/mL) for 24 h. miR-381 expression was examined by qPCR ( n = 5). ( G ) Schematic 3′UTR representation of the human VEGF-C containing miR-381 binding site. ( H ) JJ012 cells were transfected with the wt-VEGFC-3′UTR or mt-VEGFC-3′UTR plasmids for 24 h and stimulated with bFGF (30 ng/mL) for 24 h; relative luciferase/renilla activities were measured as described in the Methods section ( n = 5). ( I ) JJ012 cells were pretreated for 30 min with AG-1296 or PP2 and stimulated with bFGF for 24 h. wt-VEGFC-3′UTR relative luciferase/renilla activities were measured as described in the Methods section ( n = 5). Data are expressed as the mean ± SEM: * P

    Journal: Oncotarget

    Article Title: Basic fibroblast growth factor promotes VEGF-C-dependent lymphangiogenesis via inhibition of miR-381 in human chondrosarcoma cells

    doi: 10.18632/oncotarget.9570

    Figure Lengend Snippet: bFGF promotes VEGF-C via downregulation of miR-381 ( A ) JJ012 cells were incubated with bFGF (0–30 ng/mL) for 24 h; miR-381 expression was examined by qPCR ( n = 6). ( B and C ) JJ012 cells were transfected with miRNA control or miR-381 mimic for 24 h and stimulated with bFGF (30 ng/mL) for 24 h. VEGF-C expression was examined by qPCR and ELISA ( n = 5–7). ( D and E ) Medium was collected as CM, then applied to LECs for 24 h; capillary-like structure formation and in vitro cell migration in LECs was examined by tube formation and the Transwell assay (Scar bar = 100 μm) ( n = 5–7). ( F ) Cells were pretreated for 30 min with AG-1296 or PP2 and stimulated with bFGF (30 ng/mL) for 24 h. miR-381 expression was examined by qPCR ( n = 5). ( G ) Schematic 3′UTR representation of the human VEGF-C containing miR-381 binding site. ( H ) JJ012 cells were transfected with the wt-VEGFC-3′UTR or mt-VEGFC-3′UTR plasmids for 24 h and stimulated with bFGF (30 ng/mL) for 24 h; relative luciferase/renilla activities were measured as described in the Methods section ( n = 5). ( I ) JJ012 cells were pretreated for 30 min with AG-1296 or PP2 and stimulated with bFGF for 24 h. wt-VEGFC-3′UTR relative luciferase/renilla activities were measured as described in the Methods section ( n = 5). Data are expressed as the mean ± SEM: * P

    Article Snippet: Concentrations of VEGF-C in the medium were assayed using the VEGF-C enzyme immunoassay kit (R & D Systems; Minneapolis, MN, USA), according to manufacturer's procedure.

    Techniques: Incubation, Expressing, Real-time Polymerase Chain Reaction, Transfection, Enzyme-linked Immunosorbent Assay, In Vitro, Migration, Transwell Assay, Binding Assay, Luciferase

    bFGF promotes the lymphangiogenesis through upregulation of VEGF-C in chondrosarcoma cells ( A and B ) JJ012 cells were incubated with bFGF (1–100 ng/mL) for 24 h, VEGF-C expression was measured by qPCR and ELISA ( n = 6–8). ( C and D ) JJ012 cells were incubated with bFGF (1–30 ng/mL) for 24 h, or pretreated for 30 min with IgG control antibody or VEGF-C antibody (1 μg/mL), followed by stimulation with bFGF (30 ng/mL) for 24 h. Medium was collected as CM, then applied to LECs for 24 h. Capillary-like structure formation and in vitro cell migration in LECs were examined by tube formation and the Transwell assay (Scar bar = 100 μm) ( n = 6–8). Data are expressed as the mean ± SEM: * P

    Journal: Oncotarget

    Article Title: Basic fibroblast growth factor promotes VEGF-C-dependent lymphangiogenesis via inhibition of miR-381 in human chondrosarcoma cells

    doi: 10.18632/oncotarget.9570

    Figure Lengend Snippet: bFGF promotes the lymphangiogenesis through upregulation of VEGF-C in chondrosarcoma cells ( A and B ) JJ012 cells were incubated with bFGF (1–100 ng/mL) for 24 h, VEGF-C expression was measured by qPCR and ELISA ( n = 6–8). ( C and D ) JJ012 cells were incubated with bFGF (1–30 ng/mL) for 24 h, or pretreated for 30 min with IgG control antibody or VEGF-C antibody (1 μg/mL), followed by stimulation with bFGF (30 ng/mL) for 24 h. Medium was collected as CM, then applied to LECs for 24 h. Capillary-like structure formation and in vitro cell migration in LECs were examined by tube formation and the Transwell assay (Scar bar = 100 μm) ( n = 6–8). Data are expressed as the mean ± SEM: * P

    Article Snippet: Concentrations of VEGF-C in the medium were assayed using the VEGF-C enzyme immunoassay kit (R & D Systems; Minneapolis, MN, USA), according to manufacturer's procedure.

    Techniques: Incubation, Expressing, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, In Vitro, Migration, Transwell Assay

    The PDGFR signaling pathway is involved in bFGF-induced VEGF-C expression ( A ) JJ012 cells were incubated with bFGF (30 ng/mL) for the indicated time intervals; PDGFR phosphorylation was examined by western blotting ( n = 5). ( B – E ) JJ012 cells were pretreated for 30 min with AG-1296 (3 μM) or transfected with PDGFR siRNA for 24 h, followed by stimulation with bFGF (30 ng/mL) for 24 h. VEGF-C expression was examined by qPCR and ELISA ( n = 5–7). Data are expressed as the mean ± SEM: * P

    Journal: Oncotarget

    Article Title: Basic fibroblast growth factor promotes VEGF-C-dependent lymphangiogenesis via inhibition of miR-381 in human chondrosarcoma cells

    doi: 10.18632/oncotarget.9570

    Figure Lengend Snippet: The PDGFR signaling pathway is involved in bFGF-induced VEGF-C expression ( A ) JJ012 cells were incubated with bFGF (30 ng/mL) for the indicated time intervals; PDGFR phosphorylation was examined by western blotting ( n = 5). ( B – E ) JJ012 cells were pretreated for 30 min with AG-1296 (3 μM) or transfected with PDGFR siRNA for 24 h, followed by stimulation with bFGF (30 ng/mL) for 24 h. VEGF-C expression was examined by qPCR and ELISA ( n = 5–7). Data are expressed as the mean ± SEM: * P

    Article Snippet: Concentrations of VEGF-C in the medium were assayed using the VEGF-C enzyme immunoassay kit (R & D Systems; Minneapolis, MN, USA), according to manufacturer's procedure.

    Techniques: Expressing, Incubation, Western Blot, Transfection, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    c-Src activation is involved in bFGF-induced VEGF-C expression ( A – D ) JJ012 cells were pretreated for 30 min with PP2 (3 μM) or transfected with c-Src siRNA for 24 h, followed by stimulation with bFGF (30 ng/mL) for 24 h. VEGF-C expression was examined by qPCR and ELISA ( n = 6–8). ( E ) JJ012 cells were incubated with bFGF (30 ng/mL) for the indicated time intervals or indicated concentrations for 30 min; c-Src phosphorylation was examined by western blotting ( n = 5). ( F ) JJ012 cells were pretreated for 30 min with PP2 (3 μM), followed by stimulation with bFGF (30 ng/mL) for 24 h; c-Src phosphorylation was examined by western blotting ( n = 5). Data are expressed as the mean ± SEM: * P

    Journal: Oncotarget

    Article Title: Basic fibroblast growth factor promotes VEGF-C-dependent lymphangiogenesis via inhibition of miR-381 in human chondrosarcoma cells

    doi: 10.18632/oncotarget.9570

    Figure Lengend Snippet: c-Src activation is involved in bFGF-induced VEGF-C expression ( A – D ) JJ012 cells were pretreated for 30 min with PP2 (3 μM) or transfected with c-Src siRNA for 24 h, followed by stimulation with bFGF (30 ng/mL) for 24 h. VEGF-C expression was examined by qPCR and ELISA ( n = 6–8). ( E ) JJ012 cells were incubated with bFGF (30 ng/mL) for the indicated time intervals or indicated concentrations for 30 min; c-Src phosphorylation was examined by western blotting ( n = 5). ( F ) JJ012 cells were pretreated for 30 min with PP2 (3 μM), followed by stimulation with bFGF (30 ng/mL) for 24 h; c-Src phosphorylation was examined by western blotting ( n = 5). Data are expressed as the mean ± SEM: * P

    Article Snippet: Concentrations of VEGF-C in the medium were assayed using the VEGF-C enzyme immunoassay kit (R & D Systems; Minneapolis, MN, USA), according to manufacturer's procedure.

    Techniques: Activation Assay, Expressing, Transfection, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Incubation, Western Blot

    bFGF knockdown in chondrosarcomas decreases lymphangiogenesis in vivo ( A – C ) VEGF-C and mR-381 expression in JJ012/control shRNA and JJ012/bFGF shRNAs were examined by qPCR, Western blotting and ELISA ( n = 3). ( D and E ) LECs were incubated with CM collected from JJ012/control shRNAs or JJ012/bFGF shRNAs for 24 h; tube formation or cell migration was examined by photographs or Transwell assay ( n = 5). ( F ) JJ012/control shRNA and JJ012/bFGF shRNA cells were mixed with Matrigel and injected into the flanks of mice, and tumors were monitored by bioluminescence imaging. ( G ) After 42 days, the tumors were embedded in paraffin and sections were immunostained using integrin LYEC and VEGF-C antibodies (Scar bar = 50 μm) ( n = 6). Data are expressed as the mean ± SEM: * P

    Journal: Oncotarget

    Article Title: Basic fibroblast growth factor promotes VEGF-C-dependent lymphangiogenesis via inhibition of miR-381 in human chondrosarcoma cells

    doi: 10.18632/oncotarget.9570

    Figure Lengend Snippet: bFGF knockdown in chondrosarcomas decreases lymphangiogenesis in vivo ( A – C ) VEGF-C and mR-381 expression in JJ012/control shRNA and JJ012/bFGF shRNAs were examined by qPCR, Western blotting and ELISA ( n = 3). ( D and E ) LECs were incubated with CM collected from JJ012/control shRNAs or JJ012/bFGF shRNAs for 24 h; tube formation or cell migration was examined by photographs or Transwell assay ( n = 5). ( F ) JJ012/control shRNA and JJ012/bFGF shRNA cells were mixed with Matrigel and injected into the flanks of mice, and tumors were monitored by bioluminescence imaging. ( G ) After 42 days, the tumors were embedded in paraffin and sections were immunostained using integrin LYEC and VEGF-C antibodies (Scar bar = 50 μm) ( n = 6). Data are expressed as the mean ± SEM: * P

    Article Snippet: Concentrations of VEGF-C in the medium were assayed using the VEGF-C enzyme immunoassay kit (R & D Systems; Minneapolis, MN, USA), according to manufacturer's procedure.

    Techniques: In Vivo, Expressing, shRNA, Real-time Polymerase Chain Reaction, Western Blot, Enzyme-linked Immunosorbent Assay, Incubation, Migration, Transwell Assay, Injection, Mouse Assay, Imaging

    Clinical significance of bFGF and VEGF-C in specimens from patients with chondrosarcoma Tumor specimens were immunostained with anti-VEGF-C antibody. Staining intensity was scored 1–5. ( A ) IHC photographs (Scar bar = 50 μm). The quantitated results are shown in ( B and C ). ( D ) Correlation between bFGF, VEGF-C, and chondrosarcoma clinical grades. Data are expressed as the mean ± SEM.

    Journal: Oncotarget

    Article Title: Basic fibroblast growth factor promotes VEGF-C-dependent lymphangiogenesis via inhibition of miR-381 in human chondrosarcoma cells

    doi: 10.18632/oncotarget.9570

    Figure Lengend Snippet: Clinical significance of bFGF and VEGF-C in specimens from patients with chondrosarcoma Tumor specimens were immunostained with anti-VEGF-C antibody. Staining intensity was scored 1–5. ( A ) IHC photographs (Scar bar = 50 μm). The quantitated results are shown in ( B and C ). ( D ) Correlation between bFGF, VEGF-C, and chondrosarcoma clinical grades. Data are expressed as the mean ± SEM.

    Article Snippet: Concentrations of VEGF-C in the medium were assayed using the VEGF-C enzyme immunoassay kit (R & D Systems; Minneapolis, MN, USA), according to manufacturer's procedure.

    Techniques: Staining, Immunohistochemistry

    Cytochrome P450 1B1-deficient ( Cyp1b1 −/− ) retinal astrocytes (ACs) express reduced levels of inflammatory mediators. A – C : expression levels of various inflammatory factors assessed by real-time quantitative (q)PCR analysis: bone morphogenetic protein-7 (BMP-7) ( A ); monocyte chemoattractant protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), and neuronal nitric oxide synthase (nNOS) ( B ); and IL-1β, IL-6, INF-γ, and TNF-α ( C ). D : VEGF-A amounts determined by ELISA in both conditioned medium (CM) and AC lysates (CML). E : expression levels of various VEGF-A isoforms determined by real-time qPCR. Please note a significant decrease in the levels of BMP-7 and MCP-1 (** P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: Cyp1b1-deficient retinal astrocytes are more proliferative and migratory and are protected from oxidative stress and inflammation

    doi: 10.1152/ajpcell.00021.2019

    Figure Lengend Snippet: Cytochrome P450 1B1-deficient ( Cyp1b1 −/− ) retinal astrocytes (ACs) express reduced levels of inflammatory mediators. A – C : expression levels of various inflammatory factors assessed by real-time quantitative (q)PCR analysis: bone morphogenetic protein-7 (BMP-7) ( A ); monocyte chemoattractant protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), and neuronal nitric oxide synthase (nNOS) ( B ); and IL-1β, IL-6, INF-γ, and TNF-α ( C ). D : VEGF-A amounts determined by ELISA in both conditioned medium (CM) and AC lysates (CML). E : expression levels of various VEGF-A isoforms determined by real-time qPCR. Please note a significant decrease in the levels of BMP-7 and MCP-1 (** P

    Article Snippet: The amount of VEGF secreted by Cyp1b1 +/+ and Cyp1b1 −/− retinal ACs was determined using Mouse VEGF Immunoassay kit (R & D Systems).

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction

    VEGF-A was another downstream proangiogenic factor of caspase 3 A. ELISA showing that VEGF-A concentrations of CM collected from 10 Gy-irradiated U87 cells treated with caspase 3 inhibitor, Z-DEVD-FMK, was much lower than controls. B. p-eIF4E induction in response to irradiation was inhibited when caspase 3 was inactivated. C. Ki8751, a VEGFR2 inhibitor, significantly mitigated the proliferation-stimulating effect of dying U87 cells on HUVEC-Fluc. D. Left panel, quantification analysis showing that Ki8751 decreased HUVEC migration towards CM from irradiated U87 cells. Right panel, representative images of HUVEC migration with or without administration of Ki8751 towards CM from irradiated U87 cells. Scale bar: 250 μm. E. A schematic representation of mechanisms underlying post-irradiation angiogenesis elicited by dying glioma cells.

    Journal: Cancer letters

    Article Title: Dying glioma cells establish a proangiogenic microenvironment through a caspase 3 dependent mechanism

    doi: 10.1016/j.canlet.2016.10.042

    Figure Lengend Snippet: VEGF-A was another downstream proangiogenic factor of caspase 3 A. ELISA showing that VEGF-A concentrations of CM collected from 10 Gy-irradiated U87 cells treated with caspase 3 inhibitor, Z-DEVD-FMK, was much lower than controls. B. p-eIF4E induction in response to irradiation was inhibited when caspase 3 was inactivated. C. Ki8751, a VEGFR2 inhibitor, significantly mitigated the proliferation-stimulating effect of dying U87 cells on HUVEC-Fluc. D. Left panel, quantification analysis showing that Ki8751 decreased HUVEC migration towards CM from irradiated U87 cells. Right panel, representative images of HUVEC migration with or without administration of Ki8751 towards CM from irradiated U87 cells. Scale bar: 250 μm. E. A schematic representation of mechanisms underlying post-irradiation angiogenesis elicited by dying glioma cells.

    Article Snippet: To detect the VEGF-A concentration of supernatants, we used Human VEGF Valukine ELISA Kit (VAL106; R & D Systems, MN, USA).

    Techniques: Enzyme-linked Immunosorbent Assay, Irradiation, Migration

    Metformin prevents the NGF induced VEGF expression and angiogenic properties of ovarian cells. Ovarian cells were treated with metformin 10 mM for 48 h and/or NGF 100 ng/mL or 150 ng/mL (A2780/HOSE cells and SKOV3 cells, respectively) for 24 h or the last 2 h, and then processed to detect VEGF expression. ( A , C , E ) Representative agarose gels with PCR products of different VEGF transcripts (VEGF 121, VEGF 165 and VEGF 189 amino acids) in ovarian cells. Semi-quantification of N = 4 or more independent experiments. ( B , D , F ) VEGF detection in the culture supernatants of ovarian cells by enzyme-linked immunosorbent assay (ELISA). N = 4 or more independent experiments induplicate. ( G , H ) Angiogenic score calculated as indicated in the methodology section with conditioned medium from A2780 or SKOV3 cells, respectively. Bar = 50 µm. N = 4 or more independent experiments (4–8 images were evaluated per experiment). * p

    Journal: Pharmaceuticals

    Article Title: Metformin Reduces NGF-Induced Tumour Promoter Effects in Epithelial Ovarian Cancer Cells

    doi: 10.3390/ph13100315

    Figure Lengend Snippet: Metformin prevents the NGF induced VEGF expression and angiogenic properties of ovarian cells. Ovarian cells were treated with metformin 10 mM for 48 h and/or NGF 100 ng/mL or 150 ng/mL (A2780/HOSE cells and SKOV3 cells, respectively) for 24 h or the last 2 h, and then processed to detect VEGF expression. ( A , C , E ) Representative agarose gels with PCR products of different VEGF transcripts (VEGF 121, VEGF 165 and VEGF 189 amino acids) in ovarian cells. Semi-quantification of N = 4 or more independent experiments. ( B , D , F ) VEGF detection in the culture supernatants of ovarian cells by enzyme-linked immunosorbent assay (ELISA). N = 4 or more independent experiments induplicate. ( G , H ) Angiogenic score calculated as indicated in the methodology section with conditioned medium from A2780 or SKOV3 cells, respectively. Bar = 50 µm. N = 4 or more independent experiments (4–8 images were evaluated per experiment). * p

    Article Snippet: VEGF DeterminationVEGF levels in culture supernatants were determined with an enzyme immunosorbent assay (ELISA) Kit (R & D Systems, #DVE00), according to the manufacturer’s instructions.

    Techniques: Expressing, Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay