antibodies against vegf a  (Abcam)

 
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 95
    Name:
    Anti VEGFA antibody VG76e
    Description:

    Catalog Number:
    ab119
    Price:
    None
    Buy from Supplier


    Structured Review

    Abcam antibodies against vegf a
    Relative <t>VEGF-A,</t> VEGF-B, VEGF-R, HIF-1A, and PECAM RNA levels in hernia and control ASCs by QRT-PCR, after 12 hours of incubation in hypoxic conditions. Hernia ASCs in blue and control ASCs in light blue.

    https://www.bioz.com/result/antibodies against vegf a/product/Abcam
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against vegf a - by Bioz Stars, 2021-03
    95/100 stars

    Images

    1) Product Images from "Adipose-Derived Mesenchymal Stem Cells from Ventral Hernia Repair Patients Demonstrate Decreased Vasculogenesis"

    Article Title: Adipose-Derived Mesenchymal Stem Cells from Ventral Hernia Repair Patients Demonstrate Decreased Vasculogenesis

    Journal: BioMed Research International

    doi: 10.1155/2014/983715

    Relative VEGF-A, VEGF-B, VEGF-R, HIF-1A, and PECAM RNA levels in hernia and control ASCs by QRT-PCR, after 12 hours of incubation in hypoxic conditions. Hernia ASCs in blue and control ASCs in light blue.
    Figure Legend Snippet: Relative VEGF-A, VEGF-B, VEGF-R, HIF-1A, and PECAM RNA levels in hernia and control ASCs by QRT-PCR, after 12 hours of incubation in hypoxic conditions. Hernia ASCs in blue and control ASCs in light blue.

    Techniques Used: Quantitative RT-PCR, Incubation

    Relative VEGF-A protein expression in hernia and control ASCs by western blotting, after 0 and 3 days of growth in differentiation media. Hernia ASCs in blue and control ASCs in light blue.
    Figure Legend Snippet: Relative VEGF-A protein expression in hernia and control ASCs by western blotting, after 0 and 3 days of growth in differentiation media. Hernia ASCs in blue and control ASCs in light blue.

    Techniques Used: Expressing, Western Blot

    Relative VEGF-A protein expression in hernia and control ASCs by western blotting, after 0, 12, and 24 hours of incubation in hypoxic conditions. Hernia ASCs in blue and control ASCs in light blue.
    Figure Legend Snippet: Relative VEGF-A protein expression in hernia and control ASCs by western blotting, after 0, 12, and 24 hours of incubation in hypoxic conditions. Hernia ASCs in blue and control ASCs in light blue.

    Techniques Used: Expressing, Western Blot, Incubation

    2) Product Images from "Tubeimoside-1 inhibits the proliferation and metastasis by promoting miR-126-5p expression in non-small cell lung cancer cellsNF-kB, JNK and p53 pathways are involved in tubeimoside-1-induced apoptosis in HepG2 cells with oxidative stress and G ("

    Article Title: Tubeimoside-1 inhibits the proliferation and metastasis by promoting miR-126-5p expression in non-small cell lung cancer cellsNF-kB, JNK and p53 pathways are involved in tubeimoside-1-induced apoptosis in HepG2 cells with oxidative stress and G (

    Journal: Oncology Letters

    doi: 10.3892/ol.2018.9051

    TBMS1 downregulates the expression of miR-126-5p-targeted VEGF-A (A) The 3′UTR sequence of VEGF-A and its binding site on miR-126-5p. (B) RT-PCR detection of VEGF-A mRNA expression in TBMS1-treated NCI-H1299 cells. Data in each group are expressed as mean ± SD from three independent experiments. β-actin was used as an internal control. Compared with control, ***P
    Figure Legend Snippet: TBMS1 downregulates the expression of miR-126-5p-targeted VEGF-A (A) The 3′UTR sequence of VEGF-A and its binding site on miR-126-5p. (B) RT-PCR detection of VEGF-A mRNA expression in TBMS1-treated NCI-H1299 cells. Data in each group are expressed as mean ± SD from three independent experiments. β-actin was used as an internal control. Compared with control, ***P

    Techniques Used: Expressing, Sequencing, Binding Assay, Reverse Transcription Polymerase Chain Reaction

    3) Product Images from "Angiotensin-(1–7) Suppresses Hepatocellular Carcinoma Growth and Angiogenesis via Complex Interactions of Angiotensin II Type 1 Receptor, Angiotensin II Type 2 Receptor and Mas Receptor"

    Article Title: Angiotensin-(1–7) Suppresses Hepatocellular Carcinoma Growth and Angiogenesis via Complex Interactions of Angiotensin II Type 1 Receptor, Angiotensin II Type 2 Receptor and Mas Receptor

    Journal: Molecular Medicine

    doi: 10.2119/molmed.2015.00022

    ) on H22 cell–endothelial cell communication in vitro ), VEGF-A and H22 medium, respectively. * P
    Figure Legend Snippet: ) on H22 cell–endothelial cell communication in vitro ), VEGF-A and H22 medium, respectively. * P

    Techniques Used: In Vitro

    4) Product Images from "Xuan Bi Tong Yu Fang Promotes Angiogenesis via VEGF-Notch1/Dll4 Pathway in Myocardial Ischemic Rats"

    Article Title: Xuan Bi Tong Yu Fang Promotes Angiogenesis via VEGF-Notch1/Dll4 Pathway in Myocardial Ischemic Rats

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    doi: 10.1155/2020/5041629

    Protein expression of VEGF, Notch1, and Dll4 was measured by western blot. Compared with the model group, the expression of Notch1 and Dll4 was significantly decreased by XBTYF at all doses (3.2, 1.6, and 0.8 g/kg), whereas that of VEGF was increased. Values represent the average of three replicates, ∗ P
    Figure Legend Snippet: Protein expression of VEGF, Notch1, and Dll4 was measured by western blot. Compared with the model group, the expression of Notch1 and Dll4 was significantly decreased by XBTYF at all doses (3.2, 1.6, and 0.8 g/kg), whereas that of VEGF was increased. Values represent the average of three replicates, ∗ P

    Techniques Used: Expressing, Western Blot

    Related Articles

    Incubation:

    Article Title: The glucagon-like peptide-1 receptor agonist reduces inflammation and blood-brain barrier breakdown in an astrocyte-dependent manner in experimental stroke
    Article Snippet: Fixed cells were permeabilized with 0.3% Triton X-100 for 15 min and blocked with 10% goat serum in PBS for 1 h at RT. .. After that, sections or fixed cells were incubated at 4 °C overnight with the following primary antibodies: GFAP (CST); VEGF-A (Abcam); MMP9 (Invitrogen); claudin-5 and and ZO-1 (Invitrogen); occludin (Abcam); and GLP-1R (Bioss). .. After three washes with PBS, an Alexa Fluor 488- or 555-labeled secondary antibody (Invitrogen) was added and incubated for 1 h at RT.

    Article Title: Tumor-suppressive microRNA-218 inhibits tumor angiogenesis via targeting the mTOR component RICTOR in prostate cancer
    Article Snippet: Approximate 30 μg of protein was separated with 10% SDS–PAGE gel and blotted onto nitrocellulose membranes. .. Then membranes were blocked with 5% skim milk at room temperature for 1 hour and then incubated with primary antibodies against GAPDH (Shanghai Kangchen), RICTOR (Bethyl Laboratories), VEGFA (Abcam), Akt (Cell signaling Technology), mTOR (Cell signaling Technology), HIF1α (Abcam) and HIF2α (Abcam) at 4°C overnight, followed by TBST wash and 1 hour incubation with horseradish peroxidase-conjugated secondary antibodies at room temperature. .. Protein bands were visualized by a Molecular Imager ChemiDoc XRS System (Bio-Rad Laboratories, Hercules, CA, USA).

    Article Title: Down regulation of MiR-93 contributes to endometriosis through targeting MMP3 and VEGFA
    Article Snippet: The proteins were separated by electrophoresis, and the proteins in the gels were blotted onto PVDF membranes (Amersham Pharmacia Biotech, St. Albans, Herts, UK) by electrophoretic transfer. .. The membrane was incubated with mouse anti-VEGFA or anti-MMP3 monoclonal antibody (Abcam, Cambridge, MA, USA), and mouse anti-β-actin monoclonal antibody (Santa Cruz Biotechnology Inc., Santa Cruz, CA, USA) at 37°C for 1 h. The specific protein-antibody complex was detected by using horseradish peroxidase conjugated rabbit anti-mouse IgG. .. Chemiluminescence reaction was carried out using the ECL kit (Pierce, Appleton, WI, USA) for detection.

    Staining:

    Article Title: Neuroretinal hypoxic signaling in a new preclinical murine model for proliferative diabetic retinopathy
    Article Snippet: Immunostaining Sections were permeabilized with 0.1% Triton-X100 (Fisher Scientific, Fair Lawn, NJ, USA) in PBS (PBS-T) and blocked in 5% goat serum. .. Sections were stained with one of the following primary antibodies: CD31 (1:20; BD Biosciences, San Jose, CA, USA), VEGFA (1:1000; Abcam), HIF1α (1:500; Novus Biologicals) and VHL (1:100; Santa Cruz Biotechnology). .. Secondary antibodies were Cy3-conjugated donkey anti-Rat (Jackson ImmunoResearch Laboratories Inc., Bar Harbor, ME, USA), Alexa Fluor 488 donkey anti-rat (Invitrogen), Alexa Fluor 488 and Alexa Fluor 555 goat anti-rabbit (Invitrogen), and Alexa Fluor 555 goat anti-mouse (Invitrogen) at 1:500.

    Mouse Assay:

    Article Title: Endoplasmic reticulum resident oxidase ERO1-Lalpha promotes hepatocellular carcinoma metastasis and angiogenesis through the S1PR1/STAT3/VEGF-A pathway
    Article Snippet: .. Primary antibodies were from rabbits against S1PR1, VEGF-A (Abcam, Cambridge, UK), STAT3, p-STAT3, E-cadherin, vimentin, Slug, and GAPDH (Cell Signaling Technology, Danvers, MA, USA); and from mice against ERO1α (Santa Cruz Biotechnology, Santa Cruz, CA, USA). .. ERO1α knockdown and overexpression Commercially available lentiviral-mediated ERO1α knockdown vector or the negative control (shERO1α/shNC) and lentiviral-mediated overexpressing ERO1α vector or scrambled lentiviral construct (ERO1α/Vector) were designed and produced (GenePharma Co. Ltd Shanghai, China).

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 86
    Abcam rabbit antibodies against vegf
    Synovial tissue (ST) angiogenesis, oxidative stress and cellular bioenergetics. To support the concept that oxidative stress, angiogenesis and energy metabolism are interconnected processes that co-exist during the inflammation milieu, double-immunofluorescence staining was performed. ST slides were co-incubated with primary mouse antibody against human 4-hydroxy-2-nonenal <t>(4-HNE)</t> and with primary rabbit antibodies against angiogenic factors (vascular endothelial growth factor <t>[VEGF],</t> angiopoietin 2 [Ang2], tyrosine kinase receptor [Tie2]), glycolytic proteins (glyceraldehyde 3-phosphate dehydrogenase [GAPDH], pyruvate kinase isozyme 2 [PKM2], glucose transporter 1 [GLUT1]) and a mitochondrial marker (adenosine triphosphate synthase subunit β [ATP5B]). Representative merged immunofluorescence images demonstrate examples of co-localisation ( yellow ) of 4-HNE with VEGF, Ang2, Tie2, GAPDH, PKM2, GLUT1 and ATP5B. Cells stained green are positive for 4-HNE only; cells stained red are positive only for VEGF, Ang2, Tie2, GAPDH, PKM2, GLUT1 and ATP5B. Arrows indicate examples of co-localisation. Magnification of photomicrographs × 20, insets : Figure S4
    Rabbit Antibodies Against Vegf, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit antibodies against vegf/product/Abcam
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit antibodies against vegf - by Bioz Stars, 2021-03
    86/100 stars
      Buy from Supplier

    97
    Abcam antibodies against vegf
    SIRT1 inhibitor nicotinamide partially counteracts the effects of <t>DPP‐4</t> inhibitors on the cell proliferation, migration, production of <t>VEGF,</t> and mRNA expression of SIRT1, HIF‐1α, eNOS, and VEGF in rBMVECs under hypoxic/high‐glucose conditions. A, MTT experiment results for different groups showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the reduced cell proliferation of rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). B, Number of migratory cells in different groups showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the reduced cell migration of rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). C, ELISA experiment results showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the VEGF production in rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). D, qRT‐PCR experiment results showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the mRNA expression of SIRT1, HIF‐1α, eNOS, and VEGF in rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). The difference between groups was confirmed with statistical significance (*** P
    Antibodies Against Vegf, supplied by Abcam, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against vegf/product/Abcam
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against vegf - by Bioz Stars, 2021-03
    97/100 stars
      Buy from Supplier

    Image Search Results


    Synovial tissue (ST) angiogenesis, oxidative stress and cellular bioenergetics. To support the concept that oxidative stress, angiogenesis and energy metabolism are interconnected processes that co-exist during the inflammation milieu, double-immunofluorescence staining was performed. ST slides were co-incubated with primary mouse antibody against human 4-hydroxy-2-nonenal (4-HNE) and with primary rabbit antibodies against angiogenic factors (vascular endothelial growth factor [VEGF], angiopoietin 2 [Ang2], tyrosine kinase receptor [Tie2]), glycolytic proteins (glyceraldehyde 3-phosphate dehydrogenase [GAPDH], pyruvate kinase isozyme 2 [PKM2], glucose transporter 1 [GLUT1]) and a mitochondrial marker (adenosine triphosphate synthase subunit β [ATP5B]). Representative merged immunofluorescence images demonstrate examples of co-localisation ( yellow ) of 4-HNE with VEGF, Ang2, Tie2, GAPDH, PKM2, GLUT1 and ATP5B. Cells stained green are positive for 4-HNE only; cells stained red are positive only for VEGF, Ang2, Tie2, GAPDH, PKM2, GLUT1 and ATP5B. Arrows indicate examples of co-localisation. Magnification of photomicrographs × 20, insets : Figure S4

    Journal: Arthritis Research & Therapy

    Article Title: Oxidative stress impairs energy metabolism in primary cells and synovial tissue of patients with rheumatoid arthritis

    doi: 10.1186/s13075-018-1592-1

    Figure Lengend Snippet: Synovial tissue (ST) angiogenesis, oxidative stress and cellular bioenergetics. To support the concept that oxidative stress, angiogenesis and energy metabolism are interconnected processes that co-exist during the inflammation milieu, double-immunofluorescence staining was performed. ST slides were co-incubated with primary mouse antibody against human 4-hydroxy-2-nonenal (4-HNE) and with primary rabbit antibodies against angiogenic factors (vascular endothelial growth factor [VEGF], angiopoietin 2 [Ang2], tyrosine kinase receptor [Tie2]), glycolytic proteins (glyceraldehyde 3-phosphate dehydrogenase [GAPDH], pyruvate kinase isozyme 2 [PKM2], glucose transporter 1 [GLUT1]) and a mitochondrial marker (adenosine triphosphate synthase subunit β [ATP5B]). Representative merged immunofluorescence images demonstrate examples of co-localisation ( yellow ) of 4-HNE with VEGF, Ang2, Tie2, GAPDH, PKM2, GLUT1 and ATP5B. Cells stained green are positive for 4-HNE only; cells stained red are positive only for VEGF, Ang2, Tie2, GAPDH, PKM2, GLUT1 and ATP5B. Arrows indicate examples of co-localisation. Magnification of photomicrographs × 20, insets : Figure S4

    Article Snippet: ST sections were fixed with acetone for 10 minutes and co-incubated with primary mouse antibody against human 4-HNE (GENTAUR, Kampenhout, Belgium) and with primary rabbit antibodies against VEGF, Ang2, Tie2, ATP5B and glucose transporter 1 (GLUT1) (all from Abcam), glyceraldehyde 3-phosphate dehydrogenase (GAPDH) (Trevigen, Gaithersburg, MD, USA) and pyruvate kinase isozyme 2 (PKM2) (Abgent, San Diego, CA, USA).

    Techniques: Double Immunofluorescence Staining, Incubation, Marker, Immunofluorescence, Staining

    4-Hydroxy-2-nonenal (4-HNE) induces pro-angiogenic and pro-inflammatory mechanisms in primary rheumatoid arthritis synovial fibroblast cells (RASFC). Increased vascular endothelial growth factor (VEGF) immunofluorescence in RASFC subjected to 4-HNE compared to the basal cells and quantification of VEGF, angiopoietin 2 (Ang2), basic fibroblast growth factor (bFGF), interleukin (IL)-8, platelet-derived growth factor subunit B (PDGF-B), regulated on activation, normal T cell expressed and secreted (RANTES), intercellular adhesion molecule (ICAM) in RASFC supernatants ( n = 7) following cell culture with 4-HNE. Data are presented as mean ± SEM. * p

    Journal: Arthritis Research & Therapy

    Article Title: Oxidative stress impairs energy metabolism in primary cells and synovial tissue of patients with rheumatoid arthritis

    doi: 10.1186/s13075-018-1592-1

    Figure Lengend Snippet: 4-Hydroxy-2-nonenal (4-HNE) induces pro-angiogenic and pro-inflammatory mechanisms in primary rheumatoid arthritis synovial fibroblast cells (RASFC). Increased vascular endothelial growth factor (VEGF) immunofluorescence in RASFC subjected to 4-HNE compared to the basal cells and quantification of VEGF, angiopoietin 2 (Ang2), basic fibroblast growth factor (bFGF), interleukin (IL)-8, platelet-derived growth factor subunit B (PDGF-B), regulated on activation, normal T cell expressed and secreted (RANTES), intercellular adhesion molecule (ICAM) in RASFC supernatants ( n = 7) following cell culture with 4-HNE. Data are presented as mean ± SEM. * p

    Article Snippet: ST sections were fixed with acetone for 10 minutes and co-incubated with primary mouse antibody against human 4-HNE (GENTAUR, Kampenhout, Belgium) and with primary rabbit antibodies against VEGF, Ang2, Tie2, ATP5B and glucose transporter 1 (GLUT1) (all from Abcam), glyceraldehyde 3-phosphate dehydrogenase (GAPDH) (Trevigen, Gaithersburg, MD, USA) and pyruvate kinase isozyme 2 (PKM2) (Abgent, San Diego, CA, USA).

    Techniques: Immunofluorescence, Derivative Assay, Activation Assay, Cell Culture

    SIRT1 inhibitor nicotinamide partially counteracts the effects of DPP‐4 inhibitors on the cell proliferation, migration, production of VEGF, and mRNA expression of SIRT1, HIF‐1α, eNOS, and VEGF in rBMVECs under hypoxic/high‐glucose conditions. A, MTT experiment results for different groups showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the reduced cell proliferation of rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). B, Number of migratory cells in different groups showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the reduced cell migration of rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). C, ELISA experiment results showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the VEGF production in rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). D, qRT‐PCR experiment results showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the mRNA expression of SIRT1, HIF‐1α, eNOS, and VEGF in rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). The difference between groups was confirmed with statistical significance (*** P

    Journal: CNS Neuroscience & Therapeutics

    Article Title: DPP‐4 inhibitors promote proliferation and migration of rat brain microvascular endothelial cells under hypoxic/high‐glucose conditions, potentially through the SIRT1/HIF‐1/VEGF pathway, et al. DPP‐4 inhibitors promote proliferation and migration of rat brain microvascular endothelial cells under hypoxic/high‐glucose conditions, potentially through the SIRT1/HIF‐1/VEGF pathway

    doi: 10.1111/cns.13042

    Figure Lengend Snippet: SIRT1 inhibitor nicotinamide partially counteracts the effects of DPP‐4 inhibitors on the cell proliferation, migration, production of VEGF, and mRNA expression of SIRT1, HIF‐1α, eNOS, and VEGF in rBMVECs under hypoxic/high‐glucose conditions. A, MTT experiment results for different groups showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the reduced cell proliferation of rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). B, Number of migratory cells in different groups showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the reduced cell migration of rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). C, ELISA experiment results showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the VEGF production in rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). D, qRT‐PCR experiment results showing nicotinamide partially counteracted the effects of DPP‐4 inhibitors, for example, linagliptin and berberine, on the mRNA expression of SIRT1, HIF‐1α, eNOS, and VEGF in rBMVECs by the induction of hypoxic/high‐glucose treatment (model control). The difference between groups was confirmed with statistical significance (*** P

    Article Snippet: Antibodies against VEGF and DPP‐4 were purchased from Abcam (Cambridge, MA, USA), while HIF‐1α, eNOS, SIRT1, and GAPDH were purchased from Cell Signaling Technology (Beverly, MA, USA).

    Techniques: Migration, Expressing, MTT Assay, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

    ELISA experiment results showing that DPP‐4 inhibitors linagliptin and berberine attenuated the reduction of VEGF production in rBMVECs by the induction of hypoxic/high‐glucose conditions (model control). The difference between groups was confirmed with statistical significance (*** P

    Journal: CNS Neuroscience & Therapeutics

    Article Title: DPP‐4 inhibitors promote proliferation and migration of rat brain microvascular endothelial cells under hypoxic/high‐glucose conditions, potentially through the SIRT1/HIF‐1/VEGF pathway, et al. DPP‐4 inhibitors promote proliferation and migration of rat brain microvascular endothelial cells under hypoxic/high‐glucose conditions, potentially through the SIRT1/HIF‐1/VEGF pathway

    doi: 10.1111/cns.13042

    Figure Lengend Snippet: ELISA experiment results showing that DPP‐4 inhibitors linagliptin and berberine attenuated the reduction of VEGF production in rBMVECs by the induction of hypoxic/high‐glucose conditions (model control). The difference between groups was confirmed with statistical significance (*** P

    Article Snippet: Antibodies against VEGF and DPP‐4 were purchased from Abcam (Cambridge, MA, USA), while HIF‐1α, eNOS, SIRT1, and GAPDH were purchased from Cell Signaling Technology (Beverly, MA, USA).

    Techniques: Enzyme-linked Immunosorbent Assay

    DPP‐4 inhibitors linagliptin and berberine attenuated the reduction in mRNA and protein expressions of VEGF and eNOS in rBMVECs by the induction of hypoxic/high‐glucose conditions. A, Results of qRT‐PCR experiment showing the mRNA expression of VEGF and eNOS was reduced by the induction of hypoxic/high‐glucose treatment in rBMVECs (model control), which was attenuated to a large extent by the administration of DPP‐4 inhibitors, for example, linagliptin and berberine. B, Western blot results showing the protein expression of VEGF and eNOS was decreased by the induction of hypoxic/high‐glucose treatment in rBMVECs (model control), which was attenuated to a large extent by the administration of DPP‐4 inhibitors, for example, linagliptin and berberine. C, Quantitative results of Western blot analysis. The difference between groups was confirmed with statistical significance (*** P

    Journal: CNS Neuroscience & Therapeutics

    Article Title: DPP‐4 inhibitors promote proliferation and migration of rat brain microvascular endothelial cells under hypoxic/high‐glucose conditions, potentially through the SIRT1/HIF‐1/VEGF pathway, et al. DPP‐4 inhibitors promote proliferation and migration of rat brain microvascular endothelial cells under hypoxic/high‐glucose conditions, potentially through the SIRT1/HIF‐1/VEGF pathway

    doi: 10.1111/cns.13042

    Figure Lengend Snippet: DPP‐4 inhibitors linagliptin and berberine attenuated the reduction in mRNA and protein expressions of VEGF and eNOS in rBMVECs by the induction of hypoxic/high‐glucose conditions. A, Results of qRT‐PCR experiment showing the mRNA expression of VEGF and eNOS was reduced by the induction of hypoxic/high‐glucose treatment in rBMVECs (model control), which was attenuated to a large extent by the administration of DPP‐4 inhibitors, for example, linagliptin and berberine. B, Western blot results showing the protein expression of VEGF and eNOS was decreased by the induction of hypoxic/high‐glucose treatment in rBMVECs (model control), which was attenuated to a large extent by the administration of DPP‐4 inhibitors, for example, linagliptin and berberine. C, Quantitative results of Western blot analysis. The difference between groups was confirmed with statistical significance (*** P

    Article Snippet: Antibodies against VEGF and DPP‐4 were purchased from Abcam (Cambridge, MA, USA), while HIF‐1α, eNOS, SIRT1, and GAPDH were purchased from Cell Signaling Technology (Beverly, MA, USA).

    Techniques: Quantitative RT-PCR, Expressing, Western Blot

    Vascular endothelial growth factor receptor 2 (VEGFR-2) expression in cerebellar p6, p17 and p30 rats. (A-I) Immunostaining of calbindin positive PCs (red), VEGFR-2 (green) and cell nuclei (blue) in cryosections of rat cerebella at p6, p17, p30. VEGFR-2 receptors are localized within the soma (simple white arrowheads; A–I ) of PCs and in Bergmann glia fibers (white arrows; B ), reaching up to the MCL; exemplarily few cell nuclei are labeled in different cell layers (curved white arrowheads; B,C,E,F,H,I ). Scale bars: (A–I) 20 μm.

    Journal: Frontiers in Molecular Neuroscience

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

    doi: 10.3389/fnmol.2017.00002

    Figure Lengend Snippet: Vascular endothelial growth factor receptor 2 (VEGFR-2) expression in cerebellar p6, p17 and p30 rats. (A-I) Immunostaining of calbindin positive PCs (red), VEGFR-2 (green) and cell nuclei (blue) in cryosections of rat cerebella at p6, p17, p30. VEGFR-2 receptors are localized within the soma (simple white arrowheads; A–I ) of PCs and in Bergmann glia fibers (white arrows; B ), reaching up to the MCL; exemplarily few cell nuclei are labeled in different cell layers (curved white arrowheads; B,C,E,F,H,I ). Scale bars: (A–I) 20 μm.

    Article Snippet: p6, p17 and p30 Cerebellar Rat Cryosections After blocking and permeabilization, cryosections were incubated with primary antibodies against VEGFR-2 (rabbit, polyclonal, 1:100, ab39256; Abcam) and placed in a fridge (4°C) overnight.

    Techniques: Expressing, Immunostaining, Labeling

    mRNA expression levels in PCs. (A,B) In situ hybridization: expression of VEGFR-2 in rat cerebella at the age of p6 (A) and p30 (B) . Cryosections (15 μm) of each stage were incubated with 80 nM double-DIG-LNA TM probe (Exiqon). In p6 nearly every PC showed a positive VEGFR-2 signal. During development the expression of VEGFR-2 extremely decreases. In p30 VEGFR-2 positive PCs were hardly detectable. P6 and (C) p30 PCs were laser microdissected at 200× magnification and subjected to the method of quantitative polymerase chain reaction (qPCR) (D) . For relative quantification of KDR expression, the 2 −ΔΔCt method was conducted using the housekeeping gene GAPDH for normalization; data are provided as means ± SEM. Data were tested for significance using Student’s t -test. Significant differences are indicated by *** p

    Journal: Frontiers in Molecular Neuroscience

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

    doi: 10.3389/fnmol.2017.00002

    Figure Lengend Snippet: mRNA expression levels in PCs. (A,B) In situ hybridization: expression of VEGFR-2 in rat cerebella at the age of p6 (A) and p30 (B) . Cryosections (15 μm) of each stage were incubated with 80 nM double-DIG-LNA TM probe (Exiqon). In p6 nearly every PC showed a positive VEGFR-2 signal. During development the expression of VEGFR-2 extremely decreases. In p30 VEGFR-2 positive PCs were hardly detectable. P6 and (C) p30 PCs were laser microdissected at 200× magnification and subjected to the method of quantitative polymerase chain reaction (qPCR) (D) . For relative quantification of KDR expression, the 2 −ΔΔCt method was conducted using the housekeeping gene GAPDH for normalization; data are provided as means ± SEM. Data were tested for significance using Student’s t -test. Significant differences are indicated by *** p

    Article Snippet: p6, p17 and p30 Cerebellar Rat Cryosections After blocking and permeabilization, cryosections were incubated with primary antibodies against VEGFR-2 (rabbit, polyclonal, 1:100, ab39256; Abcam) and placed in a fridge (4°C) overnight.

    Techniques: Expressing, In Situ Hybridization, Incubation, Real-time Polymerase Chain Reaction

    Increased VEGF expression in VEGF low and VEGF high transgenic β-cells leads to islet hypervascularization. A : Representative Western blot showing higher expression of VEGF in both VEGF high and VEGF low . B : A 2.7- and 17-fold increase in VEGF protein levels were found in islets from 2-month-old VEGF low and VEGF high mice measured by ELISA, wild-type (WT) mice (white bar), transgenic VEGF low mice (gray bar), and transgenic VEGF high mice (black bar). * P

    Journal: Diabetes

    Article Title: Vascular Endothelial Growth Factor-Mediated Islet Hypervascularization and Inflammation Contribute to Progressive Reduction of ?-Cell Mass

    doi: 10.2337/db12-0134

    Figure Lengend Snippet: Increased VEGF expression in VEGF low and VEGF high transgenic β-cells leads to islet hypervascularization. A : Representative Western blot showing higher expression of VEGF in both VEGF high and VEGF low . B : A 2.7- and 17-fold increase in VEGF protein levels were found in islets from 2-month-old VEGF low and VEGF high mice measured by ELISA, wild-type (WT) mice (white bar), transgenic VEGF low mice (gray bar), and transgenic VEGF high mice (black bar). * P

    Article Snippet: Proteins (50–100 µg) were separated by 10% SDS-PAGE, transferred to polyvinylidene difluoride membranes, and probed with primary antibodies against VEGF (Abcam), E-cadherin (Santa Cruz Biotechnology), and β-actin (Abcam) overnight at 4°C.

    Techniques: Expressing, Transgenic Assay, Western Blot, Mouse Assay, Enzyme-linked Immunosorbent Assay

    Two-month-old VEGF low and VEGF high mice showed disorganization of islet architecture, but normal β-cell mass. A : Top panel : immunohistochemical analysis of insulin (green) and glucagon (red). In transgenic mice, islets appeared disorganized with α-cells in the core. Bottom panel : insulin immunostaining used to visualize islet architecture. B : β-Cell mass was measured in 2-month-old mice ( n = 4–7/group): wild-type (WT) mice (white bar), transgenic VEGF low mice (gray bar), and transgenic VEGF high mice (black bar). C : Ki67 (green) and insulin (red) immunostaining were used to label proliferating β-cells (arrow). D : Percentage of Ki67-positive (replicative) β-cells. E : TUNEL (green) and insulin (red) immunostaining showed apoptotic nuclei (arrow). F : Quantification of TUNEL-positive (apoptotic) β-cells. G and H : Western blot analysis of E-cadherin using islet homogenates from 2-month-old mice. G : A representative immunoblot is shown. H : Densitometric analysis of three different immunoblots: WT mice (white bar), transgenic VEGF low mice (gray bar), and transgenic VEGF high mice (black bar). Scale bars, 100 µm. * P

    Journal: Diabetes

    Article Title: Vascular Endothelial Growth Factor-Mediated Islet Hypervascularization and Inflammation Contribute to Progressive Reduction of ?-Cell Mass

    doi: 10.2337/db12-0134

    Figure Lengend Snippet: Two-month-old VEGF low and VEGF high mice showed disorganization of islet architecture, but normal β-cell mass. A : Top panel : immunohistochemical analysis of insulin (green) and glucagon (red). In transgenic mice, islets appeared disorganized with α-cells in the core. Bottom panel : insulin immunostaining used to visualize islet architecture. B : β-Cell mass was measured in 2-month-old mice ( n = 4–7/group): wild-type (WT) mice (white bar), transgenic VEGF low mice (gray bar), and transgenic VEGF high mice (black bar). C : Ki67 (green) and insulin (red) immunostaining were used to label proliferating β-cells (arrow). D : Percentage of Ki67-positive (replicative) β-cells. E : TUNEL (green) and insulin (red) immunostaining showed apoptotic nuclei (arrow). F : Quantification of TUNEL-positive (apoptotic) β-cells. G and H : Western blot analysis of E-cadherin using islet homogenates from 2-month-old mice. G : A representative immunoblot is shown. H : Densitometric analysis of three different immunoblots: WT mice (white bar), transgenic VEGF low mice (gray bar), and transgenic VEGF high mice (black bar). Scale bars, 100 µm. * P

    Article Snippet: Proteins (50–100 µg) were separated by 10% SDS-PAGE, transferred to polyvinylidene difluoride membranes, and probed with primary antibodies against VEGF (Abcam), E-cadherin (Santa Cruz Biotechnology), and β-actin (Abcam) overnight at 4°C.

    Techniques: Mouse Assay, Immunohistochemistry, Transgenic Assay, Immunostaining, TUNEL Assay, Western Blot

    AAV-mediated VEGF overexpression in β-cells increased islet vascularization and inflammation. Two-month-old wild-type (WT) mice were injected with VEGF-expressing (AAV9-VEGF) or nonexpressing (null) AAV9 vectors (10 12 vector genomes/mouse). A : Ten days after AAV injection vasculature structure was revealed by immunostaining for collagen IV (red) and insulin (green) ( top panel ). VEGF-treated islets showed increased basement membrane compared with AAV-null. FITC-dextran (green) together with insulin (red) immunostaining was used to label functional blood vessels ( top middle panel ). Insulin (green) and glucagon (red) expression showed islet disorganization ( bottom middle panel ). Macrophage infiltration in AAV-VEGF–treated animals was determined by Mac-2 immunostaining 10 days after AAV injection ( bottom panel ). Scale bars, 100 µm. B : AAV-VEGF–injected animals showed increased Mac-2–positive area/islet area when compared with AAV-null–treated mice as early as 10 days after injection: AAV-null–treated mice (white bar) and AAV-VEGF–treated mice (black bar) ( n = 4 mice/group). C : Fed blood glucose levels were determined before AAV injection (day 0) and at several time points thereafter: AAV-null-treated mice (white circle) and AAV-VEGF–treated mice (black square) ( n = 10 mice/group). D : Glucose tolerance was measured 20 days after AAV administration (2 g/kg body weight) ( n = 10 animals/group). * P

    Journal: Diabetes

    Article Title: Vascular Endothelial Growth Factor-Mediated Islet Hypervascularization and Inflammation Contribute to Progressive Reduction of ?-Cell Mass

    doi: 10.2337/db12-0134

    Figure Lengend Snippet: AAV-mediated VEGF overexpression in β-cells increased islet vascularization and inflammation. Two-month-old wild-type (WT) mice were injected with VEGF-expressing (AAV9-VEGF) or nonexpressing (null) AAV9 vectors (10 12 vector genomes/mouse). A : Ten days after AAV injection vasculature structure was revealed by immunostaining for collagen IV (red) and insulin (green) ( top panel ). VEGF-treated islets showed increased basement membrane compared with AAV-null. FITC-dextran (green) together with insulin (red) immunostaining was used to label functional blood vessels ( top middle panel ). Insulin (green) and glucagon (red) expression showed islet disorganization ( bottom middle panel ). Macrophage infiltration in AAV-VEGF–treated animals was determined by Mac-2 immunostaining 10 days after AAV injection ( bottom panel ). Scale bars, 100 µm. B : AAV-VEGF–injected animals showed increased Mac-2–positive area/islet area when compared with AAV-null–treated mice as early as 10 days after injection: AAV-null–treated mice (white bar) and AAV-VEGF–treated mice (black bar) ( n = 4 mice/group). C : Fed blood glucose levels were determined before AAV injection (day 0) and at several time points thereafter: AAV-null-treated mice (white circle) and AAV-VEGF–treated mice (black square) ( n = 10 mice/group). D : Glucose tolerance was measured 20 days after AAV administration (2 g/kg body weight) ( n = 10 animals/group). * P

    Article Snippet: Proteins (50–100 µg) were separated by 10% SDS-PAGE, transferred to polyvinylidene difluoride membranes, and probed with primary antibodies against VEGF (Abcam), E-cadherin (Santa Cruz Biotechnology), and β-actin (Abcam) overnight at 4°C.

    Techniques: Over Expression, Mouse Assay, Injection, Expressing, Plasmid Preparation, Immunostaining, Functional Assay