vascular endothelial growth factor vegf a Search Results


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  • 92
    Santa Cruz Biotechnology vegf
    Inhibition of <t>Ang1</t> and <t>VEGF</t> diminishes VASH1 protein-mediated angiogenesis and recovery of erectile function in the diabetic mice. ( a ) Representative intracavernous (ICP) responses for the age-matched control and streptozotocin-induced diabetic mice stimulated at 2 weeks after repeated intracavernous injections of PBS + dimeric Fc (day − 3 and 0), VASH1 protein (day − 3 and 0; 4 μg/20 μL), VASH1 protein + soluble Tie2-Fc(sTie2-Fc; 4 μg/20 μL), or VASH1 protein + VEGF trap (4 mg/kg in 20 µL PBS). The stimulus interval is indicated by a solid bar. ( b , c ) Ratios of mean maximal ICP and total ICP (area under the curve) to mean systolic blood pressure (MSBP) were calculated for each group. Each bar depicts the mean (± SE) values from N = 6 animals per group. ** P
    Vegf, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 5776 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    vegf  (Abcam)
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    Abcam vegf
    (A) Immunohistochemical staining of <t>VEGF-A</t> (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, VEGF-A expression was significantly reduced in PTHKO mice compared with in WT mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, VEGF-A expression was increased in PTHKO mice, but remained significantly lower than that in WT mice. (B) Immunohistochemical staining of <t>pVEGFR2</t> (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, a significantly smaller number of pVEGFR2-positive cells was detected in the cartilaginous callus in PTHKO mice compared with in WT mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, a large number of pVEGFR2-positive cells was observed in the cartilaginous callus in WT mice, whereas a much lower level of angiogenesis was detected in PTHKO mice. (C) Immunohistochemical staining for HIF1α (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, the expression levels of cytoplasmic HIF1α were significantly lower in PTHKO mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, HIF1α expression was increased in both groups; however, the expression remained lower in PTHKO mice compared with in WT mice. Black arrows indicate positive areas. (D) Protein expression levels of VEGF, pVEGFR2 and HIF1α were detected by western blot analysis. HIF1α, hypoxia inducible factor-1α; PTH, parathroid hormone; PTHKO, PTH knockout; pVEGFR, phosphorylated-VEGF receptor 2; VEGF, vascular endothelial growth factor; WT, wild-type.
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    Millipore vegf a
    VEGFR regulates angiogenesis and tumor VM through YAP/TAZ in vitro. a Transient knockdown of YAP and/or TAZ in MCF10A overexpressing VEGFR2 decreases expression of ANG-2 and CYR61. Western blotting exposures indicate relative expression of YAP and TAZ. b , c VEGFR2 overexpression and <t>VEGF</t> treatment increases tube formation by MCF10A through YAP/TAZ. YAP and/or TAZ were transiently knocked down by siRNA in MCF10A stably overexpressing VEGFR2 and subjected to tube-formation assay on Matrigel 48 h after transfection alongside wild type MCF10A. For some conditions, cells were stimulated with 100 ng ml −1 VEGF or were treated with 100 nM verteporfin for the duration of the tube formation assay. Representative images are shown in b . Scale bar denotes 200 μm. Total tube formation was quantified in c ( n = 3). * p
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    Thermo Fisher vegf a
    <t>VEGF-A</t> is differentially expressed in AMs in vivo in response to <t>TSLP</t> hi vs. TSLP lo tumor settings. (A) Strategy shown for the experimental design and RNA sample selection for panel B. (B) VEGF-A expression as measured by qRT-PCR analysis. 100 ng/mL recombinant TSLP was added to the AM/4T1-KD co-culture system and gene expression was quantified. (C) VEGF-A expression of AMs in vivo collected from the indicated tumor-bearing mice at 7 (left), 14 (middle) or 28 (right) days post-intravenous injection. For B and C, data were normalized to the housekeeping gene GAPDH. Then one 4T1-VC sample in panel B (n = 3 biologic replicates) or one 4T1-VC sample from each time point in panel C was set to 1.0 to determine the relative expression of the other samples. Panel C represents a total of 9 separate mice per tumor-bearing group, covering the 3 distinct time points shown. Therefore, at each time point, 3 separate mice from each cohort were analyzed, and for each mouse, 3–4 technical replicates were collected. Results represent the mean ± SEM of all replicates for each tumor-bearing group at each time point. * P
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    Cell Signaling Technology Inc vegfr 2
    CLEC14A deficiency attenuates VEGFR-3 expression, promotes <t>VEGFR-2</t> expression, and forms a CLEC14A–VEGFR-3 complex via the CLEC14A cytosolic domain in ECs.
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    Thermo Fisher gene exp vegfa hs00900055 m1
    CLEC14A deficiency attenuates VEGFR-3 expression, promotes <t>VEGFR-2</t> expression, and forms a CLEC14A–VEGFR-3 complex via the CLEC14A cytosolic domain in ECs.
    Gene Exp Vegfa Hs00900055 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 976 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    PeproTech vegf a
    FLI1 and PKC co-activation mediated hESCs differentiation into iECs a Schematic illustration of the EC differentiation strategy from hESCs. b Typical morphological images of hESC-EC differentiation on days of 0, 1, 2, and 3. Scale bar, 100 μm. c The ratio of CD31+/CD144+ cells gradually increased during induction. Columns represent the mean ± SD; n = 5 independent differentiation experiments. d Representative results of the percentage of CD31+/CD144+ cells during the induction process detected by FCM. e Overexpression of FLI1 and activation of PKC in different hESC lines (hESC-254 or hESC-137) induced iECs. f Overexpressing FLI1 with different PKC activators (PMA or prostratin) yielded iECs. g Expression levels of <t>VEGF</t> , GATA2 , CD31 and CD144 genes in hESCs, human fibroblasts (HFs), iECs and EPCs. Columns represent the mean ± SD; n = 5 independent differentiation experiments
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    Cell Signaling Technology Inc vascular endothelial growth factor
    FLI1 and PKC co-activation mediated hESCs differentiation into iECs a Schematic illustration of the EC differentiation strategy from hESCs. b Typical morphological images of hESC-EC differentiation on days of 0, 1, 2, and 3. Scale bar, 100 μm. c The ratio of CD31+/CD144+ cells gradually increased during induction. Columns represent the mean ± SD; n = 5 independent differentiation experiments. d Representative results of the percentage of CD31+/CD144+ cells during the induction process detected by FCM. e Overexpression of FLI1 and activation of PKC in different hESC lines (hESC-254 or hESC-137) induced iECs. f Overexpressing FLI1 with different PKC activators (PMA or prostratin) yielded iECs. g Expression levels of <t>VEGF</t> , GATA2 , CD31 and CD144 genes in hESCs, human fibroblasts (HFs), iECs and EPCs. Columns represent the mean ± SD; n = 5 independent differentiation experiments
    Vascular Endothelial Growth Factor, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems recombinant human vegf a
    FLI1 and PKC co-activation mediated hESCs differentiation into iECs a Schematic illustration of the EC differentiation strategy from hESCs. b Typical morphological images of hESC-EC differentiation on days of 0, 1, 2, and 3. Scale bar, 100 μm. c The ratio of CD31+/CD144+ cells gradually increased during induction. Columns represent the mean ± SD; n = 5 independent differentiation experiments. d Representative results of the percentage of CD31+/CD144+ cells during the induction process detected by FCM. e Overexpression of FLI1 and activation of PKC in different hESC lines (hESC-254 or hESC-137) induced iECs. f Overexpressing FLI1 with different PKC activators (PMA or prostratin) yielded iECs. g Expression levels of <t>VEGF</t> , GATA2 , CD31 and CD144 genes in hESCs, human fibroblasts (HFs), iECs and EPCs. Columns represent the mean ± SD; n = 5 independent differentiation experiments
    Recombinant Human Vegf A, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 279 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    4Gene fms like tyrosine kinase 4 gene
    FLI1 and PKC co-activation mediated hESCs differentiation into iECs a Schematic illustration of the EC differentiation strategy from hESCs. b Typical morphological images of hESC-EC differentiation on days of 0, 1, 2, and 3. Scale bar, 100 μm. c The ratio of CD31+/CD144+ cells gradually increased during induction. Columns represent the mean ± SD; n = 5 independent differentiation experiments. d Representative results of the percentage of CD31+/CD144+ cells during the induction process detected by FCM. e Overexpression of FLI1 and activation of PKC in different hESC lines (hESC-254 or hESC-137) induced iECs. f Overexpressing FLI1 with different PKC activators (PMA or prostratin) yielded iECs. g Expression levels of <t>VEGF</t> , GATA2 , CD31 and CD144 genes in hESCs, human fibroblasts (HFs), iECs and EPCs. Columns represent the mean ± SD; n = 5 independent differentiation experiments
    Fms Like Tyrosine Kinase 4 Gene, supplied by 4Gene, used in various techniques. Bioz Stars score: 91/100, based on 312 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology anti vegf antibody
    FLI1 and PKC co-activation mediated hESCs differentiation into iECs a Schematic illustration of the EC differentiation strategy from hESCs. b Typical morphological images of hESC-EC differentiation on days of 0, 1, 2, and 3. Scale bar, 100 μm. c The ratio of CD31+/CD144+ cells gradually increased during induction. Columns represent the mean ± SD; n = 5 independent differentiation experiments. d Representative results of the percentage of CD31+/CD144+ cells during the induction process detected by FCM. e Overexpression of FLI1 and activation of PKC in different hESC lines (hESC-254 or hESC-137) induced iECs. f Overexpressing FLI1 with different PKC activators (PMA or prostratin) yielded iECs. g Expression levels of <t>VEGF</t> , GATA2 , CD31 and CD144 genes in hESCs, human fibroblasts (HFs), iECs and EPCs. Columns represent the mean ± SD; n = 5 independent differentiation experiments
    Anti Vegf Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 98/100, based on 572 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher vascular endothelial growth factor vegf a
    FLI1 and PKC co-activation mediated hESCs differentiation into iECs a Schematic illustration of the EC differentiation strategy from hESCs. b Typical morphological images of hESC-EC differentiation on days of 0, 1, 2, and 3. Scale bar, 100 μm. c The ratio of CD31+/CD144+ cells gradually increased during induction. Columns represent the mean ± SD; n = 5 independent differentiation experiments. d Representative results of the percentage of CD31+/CD144+ cells during the induction process detected by FCM. e Overexpression of FLI1 and activation of PKC in different hESC lines (hESC-254 or hESC-137) induced iECs. f Overexpressing FLI1 with different PKC activators (PMA or prostratin) yielded iECs. g Expression levels of <t>VEGF</t> , GATA2 , CD31 and CD144 genes in hESCs, human fibroblasts (HFs), iECs and EPCs. Columns represent the mean ± SD; n = 5 independent differentiation experiments
    Vascular Endothelial Growth Factor Vegf A, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 51 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore vascular endothelial growth factor vegf
    Overexpression of γ-Syn and PrPC inhibits LS <t>174T</t> cells from adhering onto EA. (A) Cell attachment analysis of the adhesiveness of unstimulated and stimulated <t>(VEGF,</t> 20 ng/mL) LS 174T cell lines on EA. Images were taken at 100× magnification using the Eclipse TS100 inverted microscope (Nikon, New York, NY, USA). (B) Fluorescence intensity was quantified. Data were expressed as fluorescence intensity and represent the mean ± SEM (error bars) of three independent experiments. Mean values were compared using one-way ANOVA followed by LSD’s post hoc test. Asterisk indicates p
    Vascular Endothelial Growth Factor Vegf, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 513 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology vegfr 1
    α-sma, CD31, HAM56, VEFGR-1 and -2, PDGFR-β and VEGF -positive cells were found in the muscle interstitium six days after AdPDGF-B gene transfer to normoxic muscle a) α-sma positive pericytes could be found both around vascular structures (arrowheads) and in the interstitium (arrow) in AdPDGF-B transduced muscles. However, a large part of the proliferating cells in the muscle interstitium were not positive for α-sma. b) Proliferation of the interstitial cells was confirmed using Ki67 staining. Ki67 positivity was found among cells in the interstitium (arrowheads) and also in vascular wall (arrow). c) Hematoxylin-eosin staining displayed a typical fibroblast structure in some cells (arrow) and a few cells could be identified as granulocytes based on the shape of their nuclei (arrowhead). d) RAM11 positive macrophages were an example of inflammatory cells found after AdPDGF-B GT (arrowhead). e) Several monocytes were stained by HAM56 in addition to macrophages. f) CD34 only stained the endothelium of large arteries in the samples. g) CD31 positive cells are normally found as part of vascular structures (arrowheads) but in AdPDGF-B transduced muscles many could also be detected in the interstitium (arrows). h) Endogenous VEGF protein expression was detected among many of the cells in the interstitium (arrowheads) in addition to vascular cells (arrows). i) Strong PDGF-B protein expression was detected in a few, probably transduced cells (arrowheads). Lower expression levels were found in vascular structures (red arrows) and in the extracellular matrix (black arrow). j) VEGF and k) HAM56 double staining confirmed after l) merging of images that some monocytes are positive for VEGF. m) <t>VEGFR-1</t> expression was detected in endothelium (arrowheads) and in the interstitial cells (arrows). n) VEGFR-2 and o) PDGFR-β were also detected in the proliferating cells (arrows). Scale bars 100µm in all images.
    Vegfr 1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 335 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems mouse vegf
    Tumor cell proliferation and apoptosis of <t>FGF-2</t> fibrosarcomas in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, <t>anti-VEGF-,</t> imatinib- and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas ( n (Vector) = 10/11/9/9; n(FGF-2) = 10/8/10/9; P (Vector vs FGF-2)
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    R&D Systems mouse vegf r3 flt 4 antibody
    Tumor cell proliferation and apoptosis of <t>FGF-2</t> fibrosarcomas in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, <t>anti-VEGF-,</t> imatinib- and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas ( n (Vector) = 10/11/9/9; n(FGF-2) = 10/8/10/9; P (Vector vs FGF-2)
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    R&D Systems vegf protein
    Tumor cell proliferation and apoptosis of <t>FGF-2</t> fibrosarcomas in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, <t>anti-VEGF-,</t> imatinib- and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas ( n (Vector) = 10/11/9/9; n(FGF-2) = 10/8/10/9; P (Vector vs FGF-2)
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    Abcam anti vegf antibody
    Tumor cell proliferation and apoptosis of <t>FGF-2</t> fibrosarcomas in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, <t>anti-VEGF-,</t> imatinib- and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas ( n (Vector) = 10/11/9/9; n(FGF-2) = 10/8/10/9; P (Vector vs FGF-2)
    Anti Vegf Antibody, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 416 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems recombinant vegf
    Tumor cell proliferation and apoptosis of <t>FGF-2</t> fibrosarcomas in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, <t>anti-VEGF-,</t> imatinib- and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas ( n (Vector) = 10/11/9/9; n(FGF-2) = 10/8/10/9; P (Vector vs FGF-2)
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    Thermo Fisher gene exp vegfa mm00437304 m1
    Tumor cell proliferation and apoptosis of <t>FGF-2</t> fibrosarcomas in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, <t>anti-VEGF-,</t> imatinib- and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas ( n (Vector) = 10/11/9/9; n(FGF-2) = 10/8/10/9; P (Vector vs FGF-2)
    Gene Exp Vegfa Mm00437304 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 290 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems vegf
    Tumor cell proliferation and apoptosis of <t>FGF-2</t> fibrosarcomas in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, <t>anti-VEGF-,</t> imatinib- and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas ( n (Vector) = 10/11/9/9; n(FGF-2) = 10/8/10/9; P (Vector vs FGF-2)
    Vegf, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 4694 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology antibody against vegf
    Tumor cell proliferation and apoptosis of <t>FGF-2</t> fibrosarcomas in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, <t>anti-VEGF-,</t> imatinib- and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas ( n (Vector) = 10/11/9/9; n(FGF-2) = 10/8/10/9; P (Vector vs FGF-2)
    Antibody Against Vegf, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 90 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Rat VEGF AccuSignal ELISA Kit KOA0330
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    Purified recombinant Human VEGF121 protein
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    Inhibition of Ang1 and VEGF diminishes VASH1 protein-mediated angiogenesis and recovery of erectile function in the diabetic mice. ( a ) Representative intracavernous (ICP) responses for the age-matched control and streptozotocin-induced diabetic mice stimulated at 2 weeks after repeated intracavernous injections of PBS + dimeric Fc (day − 3 and 0), VASH1 protein (day − 3 and 0; 4 μg/20 μL), VASH1 protein + soluble Tie2-Fc(sTie2-Fc; 4 μg/20 μL), or VASH1 protein + VEGF trap (4 mg/kg in 20 µL PBS). The stimulus interval is indicated by a solid bar. ( b , c ) Ratios of mean maximal ICP and total ICP (area under the curve) to mean systolic blood pressure (MSBP) were calculated for each group. Each bar depicts the mean (± SE) values from N = 6 animals per group. ** P

    Journal: Scientific Reports

    Article Title: Vasohibin-1 rescues erectile function through up-regulation of angiogenic factors in the diabetic mice

    doi: 10.1038/s41598-020-80925-7

    Figure Lengend Snippet: Inhibition of Ang1 and VEGF diminishes VASH1 protein-mediated angiogenesis and recovery of erectile function in the diabetic mice. ( a ) Representative intracavernous (ICP) responses for the age-matched control and streptozotocin-induced diabetic mice stimulated at 2 weeks after repeated intracavernous injections of PBS + dimeric Fc (day − 3 and 0), VASH1 protein (day − 3 and 0; 4 μg/20 μL), VASH1 protein + soluble Tie2-Fc(sTie2-Fc; 4 μg/20 μL), or VASH1 protein + VEGF trap (4 mg/kg in 20 µL PBS). The stimulus interval is indicated by a solid bar. ( b , c ) Ratios of mean maximal ICP and total ICP (area under the curve) to mean systolic blood pressure (MSBP) were calculated for each group. Each bar depicts the mean (± SE) values from N = 6 animals per group. ** P

    Article Snippet: Frozen tissue sections (20-μm thick) were incubated with antibodies to VASH1 (Santa Cruz Biotechnology Inc., Dallas, TX USA; 1:50), FITC-conjugated isolectin B4 (IB4, Sigma-Aldrich, MO, USA; 1:50), PECAM-1 (Millipore, Temecula, CA, USA; 1:50), NG2 (Millipore; 1:50), phospho-eNOS (Ser1177, Cell Signaling, MA, USA; 1:50), occludin (NOVUS Biologicals, Centennial, CO, USA; 1:50), claudin-1 (Thermo Fisher, Waltham, Massachusetts, U.S. 1:50), Ang1 (Abcam, Cambridge, U.K.; 1:50), or VEGF (Santa Cruz Biotechnology; 1:50) at 4 °C overnight.

    Techniques: Inhibition, Mouse Assay

    VASH1 protein transfer increases the cavernous expression of angiogenic factors in diabetic mice. ( a , b ) Angiopoietin-1 (Ang1, green) and PECAM1 (red), or vascular endothelial growth factor (VEGF, green) and PECAM-1 (red) staining in cavernous tissue from age-matched control and streptozotocin-induced diabetic mice 2 weeks after receiving repeated intracavernous injections of PBS (days − 3 and 0) or VASH1 protein (days − 3 and 0; 4 μg/20 μL). Scale bar = 100 µm. ( c , d ) Ang1 and VEGF-immunopositive areas were quantified by Image J. Each bar depicts the mean (± SE) values from N = 6 animals per group. * P

    Journal: Scientific Reports

    Article Title: Vasohibin-1 rescues erectile function through up-regulation of angiogenic factors in the diabetic mice

    doi: 10.1038/s41598-020-80925-7

    Figure Lengend Snippet: VASH1 protein transfer increases the cavernous expression of angiogenic factors in diabetic mice. ( a , b ) Angiopoietin-1 (Ang1, green) and PECAM1 (red), or vascular endothelial growth factor (VEGF, green) and PECAM-1 (red) staining in cavernous tissue from age-matched control and streptozotocin-induced diabetic mice 2 weeks after receiving repeated intracavernous injections of PBS (days − 3 and 0) or VASH1 protein (days − 3 and 0; 4 μg/20 μL). Scale bar = 100 µm. ( c , d ) Ang1 and VEGF-immunopositive areas were quantified by Image J. Each bar depicts the mean (± SE) values from N = 6 animals per group. * P

    Article Snippet: Frozen tissue sections (20-μm thick) were incubated with antibodies to VASH1 (Santa Cruz Biotechnology Inc., Dallas, TX USA; 1:50), FITC-conjugated isolectin B4 (IB4, Sigma-Aldrich, MO, USA; 1:50), PECAM-1 (Millipore, Temecula, CA, USA; 1:50), NG2 (Millipore; 1:50), phospho-eNOS (Ser1177, Cell Signaling, MA, USA; 1:50), occludin (NOVUS Biologicals, Centennial, CO, USA; 1:50), claudin-1 (Thermo Fisher, Waltham, Massachusetts, U.S. 1:50), Ang1 (Abcam, Cambridge, U.K.; 1:50), or VEGF (Santa Cruz Biotechnology; 1:50) at 4 °C overnight.

    Techniques: Expressing, Mouse Assay, Staining

    (A) Immunohistochemical staining of VEGF-A (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, VEGF-A expression was significantly reduced in PTHKO mice compared with in WT mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, VEGF-A expression was increased in PTHKO mice, but remained significantly lower than that in WT mice. (B) Immunohistochemical staining of pVEGFR2 (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, a significantly smaller number of pVEGFR2-positive cells was detected in the cartilaginous callus in PTHKO mice compared with in WT mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, a large number of pVEGFR2-positive cells was observed in the cartilaginous callus in WT mice, whereas a much lower level of angiogenesis was detected in PTHKO mice. (C) Immunohistochemical staining for HIF1α (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, the expression levels of cytoplasmic HIF1α were significantly lower in PTHKO mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, HIF1α expression was increased in both groups; however, the expression remained lower in PTHKO mice compared with in WT mice. Black arrows indicate positive areas. (D) Protein expression levels of VEGF, pVEGFR2 and HIF1α were detected by western blot analysis. HIF1α, hypoxia inducible factor-1α; PTH, parathroid hormone; PTHKO, PTH knockout; pVEGFR, phosphorylated-VEGF receptor 2; VEGF, vascular endothelial growth factor; WT, wild-type.

    Journal: International Journal of Molecular Medicine

    Article Title: Lack of endogenous parathyroid hormone delays fracture healing by inhibiting vascular endothelial growth factor-mediated angiogenesis

    doi: 10.3892/ijmm.2018.3614

    Figure Lengend Snippet: (A) Immunohistochemical staining of VEGF-A (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, VEGF-A expression was significantly reduced in PTHKO mice compared with in WT mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, VEGF-A expression was increased in PTHKO mice, but remained significantly lower than that in WT mice. (B) Immunohistochemical staining of pVEGFR2 (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, a significantly smaller number of pVEGFR2-positive cells was detected in the cartilaginous callus in PTHKO mice compared with in WT mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, a large number of pVEGFR2-positive cells was observed in the cartilaginous callus in WT mice, whereas a much lower level of angiogenesis was detected in PTHKO mice. (C) Immunohistochemical staining for HIF1α (magnification, ×400) in fractures. (a) In PTHKO and (b) WT mice 1 week after fracture, the expression levels of cytoplasmic HIF1α were significantly lower in PTHKO mice. (c) In PTHKO and (d) WT mice 2 weeks after fracture, HIF1α expression was increased in both groups; however, the expression remained lower in PTHKO mice compared with in WT mice. Black arrows indicate positive areas. (D) Protein expression levels of VEGF, pVEGFR2 and HIF1α were detected by western blot analysis. HIF1α, hypoxia inducible factor-1α; PTH, parathroid hormone; PTHKO, PTH knockout; pVEGFR, phosphorylated-VEGF receptor 2; VEGF, vascular endothelial growth factor; WT, wild-type.

    Article Snippet: RUNX2 (ab76956; 1:600), HIF1α (ab8366; 1:600), pVEGF receptor 2 (pVEGFR2; ab131241; 1:200), proliferating cell nuclear antigen (PCNA; ab92552; 1:400), VEGF (ab46154; 1:200), PKA (ab75991) and pAKT monoclonal antibodies (ab81283) were purchased from Abcam (Cambridge, MA, USA).

    Techniques: Immunohistochemistry, Staining, Mouse Assay, Expressing, Western Blot, Knock-Out

    VEGFR regulates angiogenesis and tumor VM through YAP/TAZ in vitro. a Transient knockdown of YAP and/or TAZ in MCF10A overexpressing VEGFR2 decreases expression of ANG-2 and CYR61. Western blotting exposures indicate relative expression of YAP and TAZ. b , c VEGFR2 overexpression and VEGF treatment increases tube formation by MCF10A through YAP/TAZ. YAP and/or TAZ were transiently knocked down by siRNA in MCF10A stably overexpressing VEGFR2 and subjected to tube-formation assay on Matrigel 48 h after transfection alongside wild type MCF10A. For some conditions, cells were stimulated with 100 ng ml −1 VEGF or were treated with 100 nM verteporfin for the duration of the tube formation assay. Representative images are shown in b . Scale bar denotes 200 μm. Total tube formation was quantified in c ( n = 3). * p

    Journal: Nature Communications

    Article Title: A LATS biosensor screen identifies VEGFR as a regulator of the Hippo pathway in angiogenesis

    doi: 10.1038/s41467-018-03278-w

    Figure Lengend Snippet: VEGFR regulates angiogenesis and tumor VM through YAP/TAZ in vitro. a Transient knockdown of YAP and/or TAZ in MCF10A overexpressing VEGFR2 decreases expression of ANG-2 and CYR61. Western blotting exposures indicate relative expression of YAP and TAZ. b , c VEGFR2 overexpression and VEGF treatment increases tube formation by MCF10A through YAP/TAZ. YAP and/or TAZ were transiently knocked down by siRNA in MCF10A stably overexpressing VEGFR2 and subjected to tube-formation assay on Matrigel 48 h after transfection alongside wild type MCF10A. For some conditions, cells were stimulated with 100 ng ml −1 VEGF or were treated with 100 nM verteporfin for the duration of the tube formation assay. Representative images are shown in b . Scale bar denotes 200 μm. Total tube formation was quantified in c ( n = 3). * p

    Article Snippet: In some experiments, 100 ng ml−1 VEGF-A or freshly prepared VP (Sigma, SML0534) were added into the medium.

    Techniques: In Vitro, Expressing, Western Blot, Over Expression, Stable Transfection, Tube Formation Assay, Transfection

    YAP/TAZ are mediators of VEGF-induced angiogenesis ex vivo and in vivo. a – c Pharmacological inhibition of YAP/TAZ reduces angiogenesis ex vivo in a rat aorta model. Sections of aorta were cultured for 7 days in Matrigel with 100 ng ml −1 VEGF and the indicated concentrations of VP. Representative images are shown in a . Sprout area is quantified in b . Scale bar denotes 500 μm. c Immunostaining of aorta sections demonstrates that outgrowths are positive for VE-cadherin. Scale bar denotes 300 μm. Wimasis image analysis software was used to visualize sprouts ( n = 3). d Transient knockdown of YAP/TAZ or pharmacological inhibition of YAP/TAZ with VP reduces angiogenesis by HUVECs in vivo in Matrigel plug experiments. Five million cells were injected subcutaneously into mice with Matrigel and 200 ng mL −1 VEGF. VP was administered by intraperitoneal injection every other day. Plugs were excised after 1 week. Representative images are shown in the top two rows. In the bottom panels, angiogenesis in the Matrigel plugs was stained by IHC for the human endothelial cell marker hCD31. Scale bar denotes 500 μm. e YAP/TAZ inhibition reduces endogenous angiogenesis in vivo in Matrigel plug experiments. Matrigel plugs with 200 ng ml −1 VEGF were implanted subcutaneously in mice. VP was administered by intraperitoneal injection every other day. Plugs were excised after 2 weeks. Angiogenesis was assessed by IHC staining for mouse mCD31 endothelial cell marker. Scale bar denotes 500 μm. f – h YAP/TAZ inhibition diminishes angiogenesis in vivo in a mouse retinal model. Mice were injected with 1 mg kg −1 VEGF with or without 100 mg kg −1 VP at postnatal day 3 (P3) and 4 (P4). At P5, retinal blood vasculature was stained. Representative images of the retinal vessel density are shown in f , whereas g shows images of the vascular front. Scale bar denotes 100 μm f or 30 μm g . Number of filopodia (active angiogenesis) is quantified in h . Each data point represents the average of two retinas from a single mouse ( n = 4 for control, n = 3 for VP). * p

    Journal: Nature Communications

    Article Title: A LATS biosensor screen identifies VEGFR as a regulator of the Hippo pathway in angiogenesis

    doi: 10.1038/s41467-018-03278-w

    Figure Lengend Snippet: YAP/TAZ are mediators of VEGF-induced angiogenesis ex vivo and in vivo. a – c Pharmacological inhibition of YAP/TAZ reduces angiogenesis ex vivo in a rat aorta model. Sections of aorta were cultured for 7 days in Matrigel with 100 ng ml −1 VEGF and the indicated concentrations of VP. Representative images are shown in a . Sprout area is quantified in b . Scale bar denotes 500 μm. c Immunostaining of aorta sections demonstrates that outgrowths are positive for VE-cadherin. Scale bar denotes 300 μm. Wimasis image analysis software was used to visualize sprouts ( n = 3). d Transient knockdown of YAP/TAZ or pharmacological inhibition of YAP/TAZ with VP reduces angiogenesis by HUVECs in vivo in Matrigel plug experiments. Five million cells were injected subcutaneously into mice with Matrigel and 200 ng mL −1 VEGF. VP was administered by intraperitoneal injection every other day. Plugs were excised after 1 week. Representative images are shown in the top two rows. In the bottom panels, angiogenesis in the Matrigel plugs was stained by IHC for the human endothelial cell marker hCD31. Scale bar denotes 500 μm. e YAP/TAZ inhibition reduces endogenous angiogenesis in vivo in Matrigel plug experiments. Matrigel plugs with 200 ng ml −1 VEGF were implanted subcutaneously in mice. VP was administered by intraperitoneal injection every other day. Plugs were excised after 2 weeks. Angiogenesis was assessed by IHC staining for mouse mCD31 endothelial cell marker. Scale bar denotes 500 μm. f – h YAP/TAZ inhibition diminishes angiogenesis in vivo in a mouse retinal model. Mice were injected with 1 mg kg −1 VEGF with or without 100 mg kg −1 VP at postnatal day 3 (P3) and 4 (P4). At P5, retinal blood vasculature was stained. Representative images of the retinal vessel density are shown in f , whereas g shows images of the vascular front. Scale bar denotes 100 μm f or 30 μm g . Number of filopodia (active angiogenesis) is quantified in h . Each data point represents the average of two retinas from a single mouse ( n = 4 for control, n = 3 for VP). * p

    Article Snippet: In some experiments, 100 ng ml−1 VEGF-A or freshly prepared VP (Sigma, SML0534) were added into the medium.

    Techniques: Ex Vivo, In Vivo, Inhibition, Cell Culture, Immunostaining, Software, Injection, Mouse Assay, Staining, Immunohistochemistry, Marker

    Model for VEGFR and Hippo signaling in angiogenesis/VM. When VEGF binds to its receptor, VEGFR, signaling through PI3K and MAPK is initiated. This leads to the inhibition of MST/LATS and subsequent activation of YAP/TAZ. YAP and TAZ induce ANG-2 and CYR61 expression, leading to enhanced angiogenesis and vasculogenic mimicry in endothelial and tumor cell lines, respectively

    Journal: Nature Communications

    Article Title: A LATS biosensor screen identifies VEGFR as a regulator of the Hippo pathway in angiogenesis

    doi: 10.1038/s41467-018-03278-w

    Figure Lengend Snippet: Model for VEGFR and Hippo signaling in angiogenesis/VM. When VEGF binds to its receptor, VEGFR, signaling through PI3K and MAPK is initiated. This leads to the inhibition of MST/LATS and subsequent activation of YAP/TAZ. YAP and TAZ induce ANG-2 and CYR61 expression, leading to enhanced angiogenesis and vasculogenic mimicry in endothelial and tumor cell lines, respectively

    Article Snippet: In some experiments, 100 ng ml−1 VEGF-A or freshly prepared VP (Sigma, SML0534) were added into the medium.

    Techniques: Inhibition, Microscale Thermophoresis, Activation Assay, Expressing

    VEGF-A is differentially expressed in AMs in vivo in response to TSLP hi vs. TSLP lo tumor settings. (A) Strategy shown for the experimental design and RNA sample selection for panel B. (B) VEGF-A expression as measured by qRT-PCR analysis. 100 ng/mL recombinant TSLP was added to the AM/4T1-KD co-culture system and gene expression was quantified. (C) VEGF-A expression of AMs in vivo collected from the indicated tumor-bearing mice at 7 (left), 14 (middle) or 28 (right) days post-intravenous injection. For B and C, data were normalized to the housekeeping gene GAPDH. Then one 4T1-VC sample in panel B (n = 3 biologic replicates) or one 4T1-VC sample from each time point in panel C was set to 1.0 to determine the relative expression of the other samples. Panel C represents a total of 9 separate mice per tumor-bearing group, covering the 3 distinct time points shown. Therefore, at each time point, 3 separate mice from each cohort were analyzed, and for each mouse, 3–4 technical replicates were collected. Results represent the mean ± SEM of all replicates for each tumor-bearing group at each time point. * P

    Journal: Oncoimmunology

    Article Title: Tumor-derived thymic stromal lymphopoietin enhances lung metastasis through an alveolar macrophage-dependent mechanism

    doi: 10.1080/2162402X.2017.1419115

    Figure Lengend Snippet: VEGF-A is differentially expressed in AMs in vivo in response to TSLP hi vs. TSLP lo tumor settings. (A) Strategy shown for the experimental design and RNA sample selection for panel B. (B) VEGF-A expression as measured by qRT-PCR analysis. 100 ng/mL recombinant TSLP was added to the AM/4T1-KD co-culture system and gene expression was quantified. (C) VEGF-A expression of AMs in vivo collected from the indicated tumor-bearing mice at 7 (left), 14 (middle) or 28 (right) days post-intravenous injection. For B and C, data were normalized to the housekeeping gene GAPDH. Then one 4T1-VC sample in panel B (n = 3 biologic replicates) or one 4T1-VC sample from each time point in panel C was set to 1.0 to determine the relative expression of the other samples. Panel C represents a total of 9 separate mice per tumor-bearing group, covering the 3 distinct time points shown. Therefore, at each time point, 3 separate mice from each cohort were analyzed, and for each mouse, 3–4 technical replicates were collected. Results represent the mean ± SEM of all replicates for each tumor-bearing group at each time point. * P

    Article Snippet: Protein levels were measured using an ELISA kit for TSLP, VEGF-A (both eBioscience, San Diego, CA) or G-CSF (RayBiotech, Norcross, GA).

    Techniques: Affinity Magnetic Separation, In Vivo, Selection, Expressing, Quantitative RT-PCR, Recombinant, Co-Culture Assay, Mouse Assay, Injection

    CLEC14A deficiency attenuates VEGFR-3 expression, promotes VEGFR-2 expression, and forms a CLEC14A–VEGFR-3 complex via the CLEC14A cytosolic domain in ECs.

    Journal: The Journal of Clinical Investigation

    Article Title: Carbohydrate-binding protein CLEC14A regulates VEGFR-2– and VEGFR-3–dependent signals during angiogenesis and lymphangiogenesis

    doi: 10.1172/JCI85145

    Figure Lengend Snippet: CLEC14A deficiency attenuates VEGFR-3 expression, promotes VEGFR-2 expression, and forms a CLEC14A–VEGFR-3 complex via the CLEC14A cytosolic domain in ECs.

    Article Snippet: The following primary antibodies were used: CD31 (BD Pharmingen; catalog 550274); NG-2 (EMD Millipore; catalog ab5320); CLEC14A (R & D Systems, catalog AF4968; Santa Cruz Biotechnology Inc., catalogs sc-246295 and sc-246296; Abcam, catalog Ab73087); MMRN2 (Santa Cruz Biotechnology Inc.; catalog sc-54120); LYVE-1 (AngioBio; catalog 11-034); VEGFR-2 (Cell Signaling Technology; catalog 2479); p–VEGFR-3 (Cell Applications Inc.; catalog CY1115); VEGFR-3 (R & D Systems, catalogs AF349 for human and AF743 for mouse; Santa Cruz Biotechnology Inc., catalog sc321); collagen type IV (Cosmo Bio; catalog LSL-LB-1407); PH3 (EMD Millipore; catalog 66-570); FITC (catalog FD40S), α-SMA (catalog F3777), X-gal (catalog 7240-90-6), and DAPI (catalog D9542) (Sigma-Aldrich); EEA1 (Santa Cruz Biotechnology Inc.; catalog sc-33585); β-actin (Thermo Fisher Scientific; catalog MA5-15739); and phosphorylated eNOS (p-eNOS), eNOS, p–VEGFR-2, VEGFR-2, p-ERK, and ERK (Cell Signaling Technology; catalogs 9571, 9572, 2478, 2479, 9106, and 9102).

    Techniques: Expressing

    Silencing or overexpression of CLEC14A regulates the phosphoactivation of VEGFR-3 and VEGFR-2 and their downstream signaling upon stimulation with VEGF-C or VEGF-A in HDBECs.

    Journal: The Journal of Clinical Investigation

    Article Title: Carbohydrate-binding protein CLEC14A regulates VEGFR-2– and VEGFR-3–dependent signals during angiogenesis and lymphangiogenesis

    doi: 10.1172/JCI85145

    Figure Lengend Snippet: Silencing or overexpression of CLEC14A regulates the phosphoactivation of VEGFR-3 and VEGFR-2 and their downstream signaling upon stimulation with VEGF-C or VEGF-A in HDBECs.

    Article Snippet: The following primary antibodies were used: CD31 (BD Pharmingen; catalog 550274); NG-2 (EMD Millipore; catalog ab5320); CLEC14A (R & D Systems, catalog AF4968; Santa Cruz Biotechnology Inc., catalogs sc-246295 and sc-246296; Abcam, catalog Ab73087); MMRN2 (Santa Cruz Biotechnology Inc.; catalog sc-54120); LYVE-1 (AngioBio; catalog 11-034); VEGFR-2 (Cell Signaling Technology; catalog 2479); p–VEGFR-3 (Cell Applications Inc.; catalog CY1115); VEGFR-3 (R & D Systems, catalogs AF349 for human and AF743 for mouse; Santa Cruz Biotechnology Inc., catalog sc321); collagen type IV (Cosmo Bio; catalog LSL-LB-1407); PH3 (EMD Millipore; catalog 66-570); FITC (catalog FD40S), α-SMA (catalog F3777), X-gal (catalog 7240-90-6), and DAPI (catalog D9542) (Sigma-Aldrich); EEA1 (Santa Cruz Biotechnology Inc.; catalog sc-33585); β-actin (Thermo Fisher Scientific; catalog MA5-15739); and phosphorylated eNOS (p-eNOS), eNOS, p–VEGFR-2, VEGFR-2, p-ERK, and ERK (Cell Signaling Technology; catalogs 9571, 9572, 2478, 2479, 9106, and 9102).

    Techniques: Over Expression

    VEGFR-2 inhibitors suppress tumor growth, increase the number of functional vessels, and improve the survival of tumor-bearing CLEC14A-KO mice.

    Journal: The Journal of Clinical Investigation

    Article Title: Carbohydrate-binding protein CLEC14A regulates VEGFR-2– and VEGFR-3–dependent signals during angiogenesis and lymphangiogenesis

    doi: 10.1172/JCI85145

    Figure Lengend Snippet: VEGFR-2 inhibitors suppress tumor growth, increase the number of functional vessels, and improve the survival of tumor-bearing CLEC14A-KO mice.

    Article Snippet: The following primary antibodies were used: CD31 (BD Pharmingen; catalog 550274); NG-2 (EMD Millipore; catalog ab5320); CLEC14A (R & D Systems, catalog AF4968; Santa Cruz Biotechnology Inc., catalogs sc-246295 and sc-246296; Abcam, catalog Ab73087); MMRN2 (Santa Cruz Biotechnology Inc.; catalog sc-54120); LYVE-1 (AngioBio; catalog 11-034); VEGFR-2 (Cell Signaling Technology; catalog 2479); p–VEGFR-3 (Cell Applications Inc.; catalog CY1115); VEGFR-3 (R & D Systems, catalogs AF349 for human and AF743 for mouse; Santa Cruz Biotechnology Inc., catalog sc321); collagen type IV (Cosmo Bio; catalog LSL-LB-1407); PH3 (EMD Millipore; catalog 66-570); FITC (catalog FD40S), α-SMA (catalog F3777), X-gal (catalog 7240-90-6), and DAPI (catalog D9542) (Sigma-Aldrich); EEA1 (Santa Cruz Biotechnology Inc.; catalog sc-33585); β-actin (Thermo Fisher Scientific; catalog MA5-15739); and phosphorylated eNOS (p-eNOS), eNOS, p–VEGFR-2, VEGFR-2, p-ERK, and ERK (Cell Signaling Technology; catalogs 9571, 9572, 2478, 2479, 9106, and 9102).

    Techniques: Functional Assay, Mouse Assay

    FLI1 and PKC co-activation mediated hESCs differentiation into iECs a Schematic illustration of the EC differentiation strategy from hESCs. b Typical morphological images of hESC-EC differentiation on days of 0, 1, 2, and 3. Scale bar, 100 μm. c The ratio of CD31+/CD144+ cells gradually increased during induction. Columns represent the mean ± SD; n = 5 independent differentiation experiments. d Representative results of the percentage of CD31+/CD144+ cells during the induction process detected by FCM. e Overexpression of FLI1 and activation of PKC in different hESC lines (hESC-254 or hESC-137) induced iECs. f Overexpressing FLI1 with different PKC activators (PMA or prostratin) yielded iECs. g Expression levels of VEGF , GATA2 , CD31 and CD144 genes in hESCs, human fibroblasts (HFs), iECs and EPCs. Columns represent the mean ± SD; n = 5 independent differentiation experiments

    Journal: Cell Death & Disease

    Article Title: FLI1 and PKC co-activation promote highly efficient differentiation of human embryonic stem cells into endothelial-like cells

    doi: 10.1038/s41419-017-0162-9

    Figure Lengend Snippet: FLI1 and PKC co-activation mediated hESCs differentiation into iECs a Schematic illustration of the EC differentiation strategy from hESCs. b Typical morphological images of hESC-EC differentiation on days of 0, 1, 2, and 3. Scale bar, 100 μm. c The ratio of CD31+/CD144+ cells gradually increased during induction. Columns represent the mean ± SD; n = 5 independent differentiation experiments. d Representative results of the percentage of CD31+/CD144+ cells during the induction process detected by FCM. e Overexpression of FLI1 and activation of PKC in different hESC lines (hESC-254 or hESC-137) induced iECs. f Overexpressing FLI1 with different PKC activators (PMA or prostratin) yielded iECs. g Expression levels of VEGF , GATA2 , CD31 and CD144 genes in hESCs, human fibroblasts (HFs), iECs and EPCs. Columns represent the mean ± SD; n = 5 independent differentiation experiments

    Article Snippet: After 3 days, supplements were changed with 50 ng ml−1 VEGF-A (96-100-20-10, PEPROTECH).

    Techniques: Activation Assay, Over Expression, Expressing

    Overexpression of γ-Syn and PrPC inhibits LS 174T cells from adhering onto EA. (A) Cell attachment analysis of the adhesiveness of unstimulated and stimulated (VEGF, 20 ng/mL) LS 174T cell lines on EA. Images were taken at 100× magnification using the Eclipse TS100 inverted microscope (Nikon, New York, NY, USA). (B) Fluorescence intensity was quantified. Data were expressed as fluorescence intensity and represent the mean ± SEM (error bars) of three independent experiments. Mean values were compared using one-way ANOVA followed by LSD’s post hoc test. Asterisk indicates p

    Journal: PeerJ

    Article Title: Cellular prion protein and γ-synuclein overexpression in LS 174T colorectal cancer cell drives endothelial proliferation-to-differentiation switch

    doi: 10.7717/peerj.4506

    Figure Lengend Snippet: Overexpression of γ-Syn and PrPC inhibits LS 174T cells from adhering onto EA. (A) Cell attachment analysis of the adhesiveness of unstimulated and stimulated (VEGF, 20 ng/mL) LS 174T cell lines on EA. Images were taken at 100× magnification using the Eclipse TS100 inverted microscope (Nikon, New York, NY, USA). (B) Fluorescence intensity was quantified. Data were expressed as fluorescence intensity and represent the mean ± SEM (error bars) of three independent experiments. Mean values were compared using one-way ANOVA followed by LSD’s post hoc test. Asterisk indicates p

    Article Snippet: Briefly, LS 174T cell lines (1 × 106 cells/T25 flask) unstimulated or stimulated with vascular endothelial growth factor (VEGF) (Sigma-Aldrich, St. Louis, MO, USA) at 20 μg/mL for 4 h were trypsinized, centrifuged, and cell pellets were mixed with Calcein AM (Trevigen, Gaithersburg, MD, USA).

    Techniques: Over Expression, Cell Attachment Assay, Inverted Microscopy, Fluorescence

    Partial secretome analysis of conditioned media from LS 174T cell lines. (A) Angiogenesis antibody array proteome profiling of CM of LS 174T cell lines. Red boxes indicate reference spots whereas green boxes indicate negative control. Numbered yellow boxes indicate the ten angiogenic factors in the CM that yielded distinct signals, which are CXCL16 (1), DPPIV (2), TIMP-1 (3), TIMP-4 (4), angiogenin (5), IGFBP-2 (6), uPA (7), IL-8 (8), amphiregulin (9) and VEGF (10). (B) Secretion levels of different angiogenesis-related proteins in LS 174T CM, LS 174T-γ-Syn CM and LS 174T-PrP CM were analyzed with ImageJ software and presented as densitometry values. (C) The ten angiogenic factors that yielded distinct signals were relatively quantified. Data of densitometry value were expressed as relative intensity compared to LS 174T CM (set as 1) and represent the mean ± SEM (error bars) of two independent experiments. Mean values were compared using one-way ANOVA followed by LSD’s post hoc test. Asterisk indicates p

    Journal: PeerJ

    Article Title: Cellular prion protein and γ-synuclein overexpression in LS 174T colorectal cancer cell drives endothelial proliferation-to-differentiation switch

    doi: 10.7717/peerj.4506

    Figure Lengend Snippet: Partial secretome analysis of conditioned media from LS 174T cell lines. (A) Angiogenesis antibody array proteome profiling of CM of LS 174T cell lines. Red boxes indicate reference spots whereas green boxes indicate negative control. Numbered yellow boxes indicate the ten angiogenic factors in the CM that yielded distinct signals, which are CXCL16 (1), DPPIV (2), TIMP-1 (3), TIMP-4 (4), angiogenin (5), IGFBP-2 (6), uPA (7), IL-8 (8), amphiregulin (9) and VEGF (10). (B) Secretion levels of different angiogenesis-related proteins in LS 174T CM, LS 174T-γ-Syn CM and LS 174T-PrP CM were analyzed with ImageJ software and presented as densitometry values. (C) The ten angiogenic factors that yielded distinct signals were relatively quantified. Data of densitometry value were expressed as relative intensity compared to LS 174T CM (set as 1) and represent the mean ± SEM (error bars) of two independent experiments. Mean values were compared using one-way ANOVA followed by LSD’s post hoc test. Asterisk indicates p

    Article Snippet: Briefly, LS 174T cell lines (1 × 106 cells/T25 flask) unstimulated or stimulated with vascular endothelial growth factor (VEGF) (Sigma-Aldrich, St. Louis, MO, USA) at 20 μg/mL for 4 h were trypsinized, centrifuged, and cell pellets were mixed with Calcein AM (Trevigen, Gaithersburg, MD, USA).

    Techniques: Ab Array, Negative Control, Software

    α-sma, CD31, HAM56, VEFGR-1 and -2, PDGFR-β and VEGF -positive cells were found in the muscle interstitium six days after AdPDGF-B gene transfer to normoxic muscle a) α-sma positive pericytes could be found both around vascular structures (arrowheads) and in the interstitium (arrow) in AdPDGF-B transduced muscles. However, a large part of the proliferating cells in the muscle interstitium were not positive for α-sma. b) Proliferation of the interstitial cells was confirmed using Ki67 staining. Ki67 positivity was found among cells in the interstitium (arrowheads) and also in vascular wall (arrow). c) Hematoxylin-eosin staining displayed a typical fibroblast structure in some cells (arrow) and a few cells could be identified as granulocytes based on the shape of their nuclei (arrowhead). d) RAM11 positive macrophages were an example of inflammatory cells found after AdPDGF-B GT (arrowhead). e) Several monocytes were stained by HAM56 in addition to macrophages. f) CD34 only stained the endothelium of large arteries in the samples. g) CD31 positive cells are normally found as part of vascular structures (arrowheads) but in AdPDGF-B transduced muscles many could also be detected in the interstitium (arrows). h) Endogenous VEGF protein expression was detected among many of the cells in the interstitium (arrowheads) in addition to vascular cells (arrows). i) Strong PDGF-B protein expression was detected in a few, probably transduced cells (arrowheads). Lower expression levels were found in vascular structures (red arrows) and in the extracellular matrix (black arrow). j) VEGF and k) HAM56 double staining confirmed after l) merging of images that some monocytes are positive for VEGF. m) VEGFR-1 expression was detected in endothelium (arrowheads) and in the interstitial cells (arrows). n) VEGFR-2 and o) PDGFR-β were also detected in the proliferating cells (arrows). Scale bars 100µm in all images.

    Journal: Circulation research

    Article Title: VEGF-A and PDGF-B combination gene therapy prolongs angiogenic effects via recruitment of interstitial mononuclear cells and paracrine effects rather than improved pericyte coverage of angiogenic vessels

    doi: 10.1161/CIRCRESAHA.108.182287

    Figure Lengend Snippet: α-sma, CD31, HAM56, VEFGR-1 and -2, PDGFR-β and VEGF -positive cells were found in the muscle interstitium six days after AdPDGF-B gene transfer to normoxic muscle a) α-sma positive pericytes could be found both around vascular structures (arrowheads) and in the interstitium (arrow) in AdPDGF-B transduced muscles. However, a large part of the proliferating cells in the muscle interstitium were not positive for α-sma. b) Proliferation of the interstitial cells was confirmed using Ki67 staining. Ki67 positivity was found among cells in the interstitium (arrowheads) and also in vascular wall (arrow). c) Hematoxylin-eosin staining displayed a typical fibroblast structure in some cells (arrow) and a few cells could be identified as granulocytes based on the shape of their nuclei (arrowhead). d) RAM11 positive macrophages were an example of inflammatory cells found after AdPDGF-B GT (arrowhead). e) Several monocytes were stained by HAM56 in addition to macrophages. f) CD34 only stained the endothelium of large arteries in the samples. g) CD31 positive cells are normally found as part of vascular structures (arrowheads) but in AdPDGF-B transduced muscles many could also be detected in the interstitium (arrows). h) Endogenous VEGF protein expression was detected among many of the cells in the interstitium (arrowheads) in addition to vascular cells (arrows). i) Strong PDGF-B protein expression was detected in a few, probably transduced cells (arrowheads). Lower expression levels were found in vascular structures (red arrows) and in the extracellular matrix (black arrow). j) VEGF and k) HAM56 double staining confirmed after l) merging of images that some monocytes are positive for VEGF. m) VEGFR-1 expression was detected in endothelium (arrowheads) and in the interstitial cells (arrows). n) VEGFR-2 and o) PDGFR-β were also detected in the proliferating cells (arrows). Scale bars 100µm in all images.

    Article Snippet: Receptor stainings were performed using VEGFR-1 (Santa Cruz, 1:250), VEGFR-2 (RDI, 1:250) and PDGFR-β (Santa Cruz, 1:200) antibodies.

    Techniques: Staining, Expressing, Double Staining

    Tumor cell proliferation and apoptosis of FGF-2 fibrosarcomas in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, anti-VEGF-, imatinib- and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas ( n (Vector) = 10/11/9/9; n(FGF-2) = 10/8/10/9; P (Vector vs FGF-2)

    Journal: Nature Communications

    Article Title: Therapeutic paradigm of dual targeting VEGF and PDGF for effectively treating FGF-2 off-target tumors

    doi: 10.1038/s41467-020-17525-6

    Figure Lengend Snippet: Tumor cell proliferation and apoptosis of FGF-2 fibrosarcomas in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, anti-VEGF-, imatinib- and combination therapy-treated T241-vector and T241-FGF-2 fibrosarcomas ( n (Vector) = 10/11/9/9; n(FGF-2) = 10/8/10/9; P (Vector vs FGF-2)

    Article Snippet: The human FGF-2 (DFB50, R & D systems), mouse VEGF (MMV00), and mouse PDGF-BB ELISA assays (MBB00, R & D Systems) were performed according to the manufacturer’s protocol with the standard curve.

    Techniques: Staining, Plasmid Preparation

    Impact of anti-PDGFRβ on tumor growth, angiogenesis, and tumor microenvironment. a Tumor growth of T241-FGF-2 fibrosarcomas in response to anti-VEGF, anti-PDGFRβ, and anti-VEGF plus anti-PDGFRβ treatments ( n = 7/6/6/7; P (Vehicle vs combination therapy) = 0.0013). Time indicates after the start of treatment. b Microvascular density and perivascular coverage of anti-VEGF-, anti-PDGFRβ-, and anti-VEGF plus anti-PDGFRβ-treated T241-FGF-2 fibrosarcomas. Red indicates CD31 + microvessels and blue indicates NG2 + pericytes. Bar = 50 μm. c Quantification of CD31 + microvessel density ( n = 7 each; P (Vehicle vs anti-PDGFRβ) = 0.0047; P (Vehicle vs combination) = 0.0007), NG2 + pericyte coverage ( n = 7 each; P (Vehicle vs anti-PDGFRβ)

    Journal: Nature Communications

    Article Title: Therapeutic paradigm of dual targeting VEGF and PDGF for effectively treating FGF-2 off-target tumors

    doi: 10.1038/s41467-020-17525-6

    Figure Lengend Snippet: Impact of anti-PDGFRβ on tumor growth, angiogenesis, and tumor microenvironment. a Tumor growth of T241-FGF-2 fibrosarcomas in response to anti-VEGF, anti-PDGFRβ, and anti-VEGF plus anti-PDGFRβ treatments ( n = 7/6/6/7; P (Vehicle vs combination therapy) = 0.0013). Time indicates after the start of treatment. b Microvascular density and perivascular coverage of anti-VEGF-, anti-PDGFRβ-, and anti-VEGF plus anti-PDGFRβ-treated T241-FGF-2 fibrosarcomas. Red indicates CD31 + microvessels and blue indicates NG2 + pericytes. Bar = 50 μm. c Quantification of CD31 + microvessel density ( n = 7 each; P (Vehicle vs anti-PDGFRβ) = 0.0047; P (Vehicle vs combination) = 0.0007), NG2 + pericyte coverage ( n = 7 each; P (Vehicle vs anti-PDGFRβ)

    Article Snippet: The human FGF-2 (DFB50, R & D systems), mouse VEGF (MMV00), and mouse PDGF-BB ELISA assays (MBB00, R & D Systems) were performed according to the manufacturer’s protocol with the standard curve.

    Techniques:

    Survival correlation and schematic diagram of underlying mechanisms of synergistic anti-FGF-2 + tumor activity by combination therapy. a Kaplan–Meier survival of FGF-2-high vs. FGF-2-low breast cancer (BRCA, n = 246 vs. 267; P = 0.0458); b ovarian cancer (OV, n = 131 vs. 129; P = 0.0097); c bladder carcinoma (BLCA, n = 261 vs. 141; P = 0.007); d and pancreatic adenocarcinoma (PAAD, n = 57 vs. 120; P = 0.003). The log-rank test was used for statistical analysis at the endpoint. Source data are provided as a Source Data file. e Tumors often produce FGF-2 and VEGF to stimulate tumor angiogenesis. While VEGF stimulates endothelial cell proliferation, migration, and endothelial cell tip formation, FGF-2 primarily induces endothelial cell proliferation. In FGF-2 positive tumors, blocking FGF-2-triggered signaling such as inhibition of FGFR inhibits endothelial cell proliferation and angiogenesis. However, the impact of anti-FGF agents on tumor angiogenesis may be modest because tumors employ VEGF to stimulate neovascularization. Thus, VEGF plays a compensatory role in circumventing the antiangiogenic effect by FGF-2. Similarly, blocking VEGF alone in FGF-2 positive tumors may also produce a limited antitumor effect because of the compensatory effect of FGF-2. In addition, FGF-2 is a potent perivascular factor to stimulate pericyte proliferation and vascular coverage through an intimate collaboration with the PDGF-B-PDGFRβ signaling pathway. Blocking PDGFRβ alone would lead to ablation of perivascular cells from tumor vessels, permitting exposure of endothelial cells to vascular stimuli such as FGF-2 and VEGF. In supporting this view, we show that anti-PDGFRβ increases rather than reduces vascular density in FGF-2 positive tumors. Simultaneous blocking VEGF and PDGFRβ signaling pathways inhibits vascular sprouting and vascular stability, leading to vascular regression in FGF-2 positive tumors.

    Journal: Nature Communications

    Article Title: Therapeutic paradigm of dual targeting VEGF and PDGF for effectively treating FGF-2 off-target tumors

    doi: 10.1038/s41467-020-17525-6

    Figure Lengend Snippet: Survival correlation and schematic diagram of underlying mechanisms of synergistic anti-FGF-2 + tumor activity by combination therapy. a Kaplan–Meier survival of FGF-2-high vs. FGF-2-low breast cancer (BRCA, n = 246 vs. 267; P = 0.0458); b ovarian cancer (OV, n = 131 vs. 129; P = 0.0097); c bladder carcinoma (BLCA, n = 261 vs. 141; P = 0.007); d and pancreatic adenocarcinoma (PAAD, n = 57 vs. 120; P = 0.003). The log-rank test was used for statistical analysis at the endpoint. Source data are provided as a Source Data file. e Tumors often produce FGF-2 and VEGF to stimulate tumor angiogenesis. While VEGF stimulates endothelial cell proliferation, migration, and endothelial cell tip formation, FGF-2 primarily induces endothelial cell proliferation. In FGF-2 positive tumors, blocking FGF-2-triggered signaling such as inhibition of FGFR inhibits endothelial cell proliferation and angiogenesis. However, the impact of anti-FGF agents on tumor angiogenesis may be modest because tumors employ VEGF to stimulate neovascularization. Thus, VEGF plays a compensatory role in circumventing the antiangiogenic effect by FGF-2. Similarly, blocking VEGF alone in FGF-2 positive tumors may also produce a limited antitumor effect because of the compensatory effect of FGF-2. In addition, FGF-2 is a potent perivascular factor to stimulate pericyte proliferation and vascular coverage through an intimate collaboration with the PDGF-B-PDGFRβ signaling pathway. Blocking PDGFRβ alone would lead to ablation of perivascular cells from tumor vessels, permitting exposure of endothelial cells to vascular stimuli such as FGF-2 and VEGF. In supporting this view, we show that anti-PDGFRβ increases rather than reduces vascular density in FGF-2 positive tumors. Simultaneous blocking VEGF and PDGFRβ signaling pathways inhibits vascular sprouting and vascular stability, leading to vascular regression in FGF-2 positive tumors.

    Article Snippet: The human FGF-2 (DFB50, R & D systems), mouse VEGF (MMV00), and mouse PDGF-BB ELISA assays (MBB00, R & D Systems) were performed according to the manufacturer’s protocol with the standard curve.

    Techniques: Activity Assay, Migration, Blocking Assay, Inhibition

    Growth rates and angiogenesis in various drug-treated FGF - 2 + and control breast cancers. a ELISA measurement of FGF-2 levels in E0771-vector ( n = 3) and E0771-FGF-2 tumor tissues ( n = 4). P = 0.0032. b Tumor growth of E0771-vector and E0771-FGF-2 ( n = 5, 6). c Tumor growth of vehicle- and anti-VEGF-treated E0771-vector ( n = 5,6; P = 0.0002). Tumor growth rates of vehicle- and anti-VEGF-treated E0771-FGF-2 ( n = 6). d Tumor growth of vehicle- and imatinib-treated E0771-vector ( n = 5). Tumor growth rates of vehicle- and imatinib-treated E0771-FGF-2 ( n = 6). e Tumor growth of vehicle- and anti-VEGF plus imatinib-treated E0771-vector ( n = 5, 6; P = 0.0001). Tumor growth rates of vehicle- and anti-VEGF plus imatinib-treated E0771-FGF-2 ( n = 6, 8; P = 0.0010). f CD31 + microvessels (red) and NG2 + pericytes (blue) in various drug-treated E0771-vector and E0771-FGF-2 cancers. Bar = 50 μm. g Quantification of microvessels ( n = 10 each; P (Vehicle-treated-vector vs anti-VEGF-treated-vector) = 0.0009), pericyte coverage ( n = 9/9/11/12; P (Vehicle-treated-vector vs anti-VEGF-treated-vector) = 0.0374) and pericyte area ( n = 9/9/10/12) of vehicle- and anti-VEGF-treated E0771 vector and E0771-FGF-2. h Quantification of microvessels ( n = 10/11/10/10; P (Vehicle-treated-vector vs imatinib-treated-vector) = 0.0009; P (Vehicle-treated-FGF-2 vs anti-VEGF-treated-FGF-2) = 0.0453), pericyte coverage ( n = 9/9/11/11; P (Vehicle-treated-vector vs imatinib-treated-vector) = 0.0120; P (Vehicle-treated-FGF-2 vs imatinib-treated-FGF-2) = 0.0103) and pericyte area ( n = 9/11/10/11; P (Vehicle-treated-vector vs imatinib-treated-vector) = 0.0038) of vehicle- and imatinib-treated E0771-vector and E0771-FGF-2. i Quantification of microvessels ( n = 10/9/10/10; P (Vehicle-treated-vector vs combination-treated-vector) = 0.0006; P (Vehicle-treated-FGF-2 vs combination therapy-treated-FGF-2) = 0.0009), pericyte coverage ( n = 9/9/11/9; P (Vehicle-treated-vector vs combination-treated-vector) = 0.0004) and pericyte area ( n = 9/9/10/9; P (Vehicle-treated-FGF-2 vs combination-treated-FGF-2) = 0.0117) of vehicle- and anti-VEGF plus imatinib-treated E0771-vector and E0771-FGF-2 cancers. FGF-2 - = vector cancers; FGF-2 + = FGF-2 cancers; n.s. Not significant; * P

    Journal: Nature Communications

    Article Title: Therapeutic paradigm of dual targeting VEGF and PDGF for effectively treating FGF-2 off-target tumors

    doi: 10.1038/s41467-020-17525-6

    Figure Lengend Snippet: Growth rates and angiogenesis in various drug-treated FGF - 2 + and control breast cancers. a ELISA measurement of FGF-2 levels in E0771-vector ( n = 3) and E0771-FGF-2 tumor tissues ( n = 4). P = 0.0032. b Tumor growth of E0771-vector and E0771-FGF-2 ( n = 5, 6). c Tumor growth of vehicle- and anti-VEGF-treated E0771-vector ( n = 5,6; P = 0.0002). Tumor growth rates of vehicle- and anti-VEGF-treated E0771-FGF-2 ( n = 6). d Tumor growth of vehicle- and imatinib-treated E0771-vector ( n = 5). Tumor growth rates of vehicle- and imatinib-treated E0771-FGF-2 ( n = 6). e Tumor growth of vehicle- and anti-VEGF plus imatinib-treated E0771-vector ( n = 5, 6; P = 0.0001). Tumor growth rates of vehicle- and anti-VEGF plus imatinib-treated E0771-FGF-2 ( n = 6, 8; P = 0.0010). f CD31 + microvessels (red) and NG2 + pericytes (blue) in various drug-treated E0771-vector and E0771-FGF-2 cancers. Bar = 50 μm. g Quantification of microvessels ( n = 10 each; P (Vehicle-treated-vector vs anti-VEGF-treated-vector) = 0.0009), pericyte coverage ( n = 9/9/11/12; P (Vehicle-treated-vector vs anti-VEGF-treated-vector) = 0.0374) and pericyte area ( n = 9/9/10/12) of vehicle- and anti-VEGF-treated E0771 vector and E0771-FGF-2. h Quantification of microvessels ( n = 10/11/10/10; P (Vehicle-treated-vector vs imatinib-treated-vector) = 0.0009; P (Vehicle-treated-FGF-2 vs anti-VEGF-treated-FGF-2) = 0.0453), pericyte coverage ( n = 9/9/11/11; P (Vehicle-treated-vector vs imatinib-treated-vector) = 0.0120; P (Vehicle-treated-FGF-2 vs imatinib-treated-FGF-2) = 0.0103) and pericyte area ( n = 9/11/10/11; P (Vehicle-treated-vector vs imatinib-treated-vector) = 0.0038) of vehicle- and imatinib-treated E0771-vector and E0771-FGF-2. i Quantification of microvessels ( n = 10/9/10/10; P (Vehicle-treated-vector vs combination-treated-vector) = 0.0006; P (Vehicle-treated-FGF-2 vs combination therapy-treated-FGF-2) = 0.0009), pericyte coverage ( n = 9/9/11/9; P (Vehicle-treated-vector vs combination-treated-vector) = 0.0004) and pericyte area ( n = 9/9/10/9; P (Vehicle-treated-FGF-2 vs combination-treated-FGF-2) = 0.0117) of vehicle- and anti-VEGF plus imatinib-treated E0771-vector and E0771-FGF-2 cancers. FGF-2 - = vector cancers; FGF-2 + = FGF-2 cancers; n.s. Not significant; * P

    Article Snippet: The human FGF-2 (DFB50, R & D systems), mouse VEGF (MMV00), and mouse PDGF-BB ELISA assays (MBB00, R & D Systems) were performed according to the manufacturer’s protocol with the standard curve.

    Techniques: Enzyme-linked Immunosorbent Assay, Plasmid Preparation

    Vascular perfusion, vascular permeability, and tumor hypoxia. a Vascular perfusion of Rhodamine-labeled lysinated 2000 kDa dextran (blue) of various monotherapy- and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancers. Red indicates CD31 + microvessels. Bar = 50 μm. b Vascular permeability of Rhodamine-labeled lysinated 70 kDa dextran (blue) of various monotherapy- and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancers. Red indicates CD31 + microvessels. Bar = 50 μm. Arrowheads indicate extravasation of 70 kDa dextran from the tumor vasculature. c Quantification of vascular perfusion of vehicle-, anti-VEGF-, imatinib- and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancers ( n (Vector) = 9/10/10/8; n (FGF-2) = 9/9/10/8; P (Vector vs FGF-2) = 0.0037; P (Vehicle-treated vector vs anti-VEGF-treated vector) = 0.0002; P (Vehicle-treated vector vs imatinib-treated vector) = 0.0260; P (Vehicle-treated vector vs combination therapy-treated vector) = 0.0007; P (Vehicle-treated FGF-2 vs combination therapy-treated FGF-2) = 0.0012). d Quantification of vascular permeability of vehicle-, anti-VEGF-, imatinib- and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancers ( n (Vector) = 10/8/9/10; n(FGF-2) = 10/10/10/9). P (Vehicle-treated vector vs anti-VEGF-treated vector) = 0.0013, P (Vehicle-treated FGF-2 vs anti-VEGF-treated FGF-2) = 0.0280, P (Vehicle-treated vector vs imatinib-treated vector) = 0.0067, P (Vehicle-treated FGF-2 vs imatinib-treated FGF-2) = 0.0066, P (Vehicle-treated vector vs combination therapy-treated vector) = 0.0077, P (Vehicle-treated FGF-2 vs combination therapy-treated FGF-2)

    Journal: Nature Communications

    Article Title: Therapeutic paradigm of dual targeting VEGF and PDGF for effectively treating FGF-2 off-target tumors

    doi: 10.1038/s41467-020-17525-6

    Figure Lengend Snippet: Vascular perfusion, vascular permeability, and tumor hypoxia. a Vascular perfusion of Rhodamine-labeled lysinated 2000 kDa dextran (blue) of various monotherapy- and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancers. Red indicates CD31 + microvessels. Bar = 50 μm. b Vascular permeability of Rhodamine-labeled lysinated 70 kDa dextran (blue) of various monotherapy- and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancers. Red indicates CD31 + microvessels. Bar = 50 μm. Arrowheads indicate extravasation of 70 kDa dextran from the tumor vasculature. c Quantification of vascular perfusion of vehicle-, anti-VEGF-, imatinib- and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancers ( n (Vector) = 9/10/10/8; n (FGF-2) = 9/9/10/8; P (Vector vs FGF-2) = 0.0037; P (Vehicle-treated vector vs anti-VEGF-treated vector) = 0.0002; P (Vehicle-treated vector vs imatinib-treated vector) = 0.0260; P (Vehicle-treated vector vs combination therapy-treated vector) = 0.0007; P (Vehicle-treated FGF-2 vs combination therapy-treated FGF-2) = 0.0012). d Quantification of vascular permeability of vehicle-, anti-VEGF-, imatinib- and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancers ( n (Vector) = 10/8/9/10; n(FGF-2) = 10/10/10/9). P (Vehicle-treated vector vs anti-VEGF-treated vector) = 0.0013, P (Vehicle-treated FGF-2 vs anti-VEGF-treated FGF-2) = 0.0280, P (Vehicle-treated vector vs imatinib-treated vector) = 0.0067, P (Vehicle-treated FGF-2 vs imatinib-treated FGF-2) = 0.0066, P (Vehicle-treated vector vs combination therapy-treated vector) = 0.0077, P (Vehicle-treated FGF-2 vs combination therapy-treated FGF-2)

    Article Snippet: The human FGF-2 (DFB50, R & D systems), mouse VEGF (MMV00), and mouse PDGF-BB ELISA assays (MBB00, R & D Systems) were performed according to the manufacturer’s protocol with the standard curve.

    Techniques: Permeability, Labeling, Plasmid Preparation

    Tumor growth rates, vascular function, and hypoxia in various drug-treated FGF - 2 + and control fibrosarcomas. a Expression levels of FGF-2 protein in T241-vector and T241-FGF-2 tumors ( n = 3; P (Vector vs FGF-2) = 0.0012). b Tumor growth of vehicle- and anti-VEGF-treated T241-vector ( n = 7, 10) and T241-FGF-2 ( n = 6; P (Vehicle-treated-vector vs anti-VEGF-treated-vector)

    Journal: Nature Communications

    Article Title: Therapeutic paradigm of dual targeting VEGF and PDGF for effectively treating FGF-2 off-target tumors

    doi: 10.1038/s41467-020-17525-6

    Figure Lengend Snippet: Tumor growth rates, vascular function, and hypoxia in various drug-treated FGF - 2 + and control fibrosarcomas. a Expression levels of FGF-2 protein in T241-vector and T241-FGF-2 tumors ( n = 3; P (Vector vs FGF-2) = 0.0012). b Tumor growth of vehicle- and anti-VEGF-treated T241-vector ( n = 7, 10) and T241-FGF-2 ( n = 6; P (Vehicle-treated-vector vs anti-VEGF-treated-vector)

    Article Snippet: The human FGF-2 (DFB50, R & D systems), mouse VEGF (MMV00), and mouse PDGF-BB ELISA assays (MBB00, R & D Systems) were performed according to the manufacturer’s protocol with the standard curve.

    Techniques: Expressing, Plasmid Preparation

    Tumor cell proliferation and apoptosis of FGF-2 breast cancers in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancer tissues. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, anti-VEGF-, imatinib- and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancers ( n (Vector) = 10/9/9/9; n(FGF-2) =10/8/8/8; P (Vector vs FGF-2) = 0.0019; P (Vehicle-treated vector vs anti-VEGF-treated vector) = 0.0063; P (Vehicle-treated vector vs imatinib-treated vector) = 0.0135; P (Vehicle-treated vector vs the combination therapy-treated vector)

    Journal: Nature Communications

    Article Title: Therapeutic paradigm of dual targeting VEGF and PDGF for effectively treating FGF-2 off-target tumors

    doi: 10.1038/s41467-020-17525-6

    Figure Lengend Snippet: Tumor cell proliferation and apoptosis of FGF-2 breast cancers in response to various drug treatment. a Ki67 + proliferative cell signals (green) co-stained with CD31 + microvessels (red) and DAPI (blue) of various monotherapy and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancer tissues. Bar = 50 μm. b Quantification of Ki67 + signals in vehicle-, anti-VEGF-, imatinib- and combination therapy-treated E0771-vector and E0771-FGF-2 breast cancers ( n (Vector) = 10/9/9/9; n(FGF-2) =10/8/8/8; P (Vector vs FGF-2) = 0.0019; P (Vehicle-treated vector vs anti-VEGF-treated vector) = 0.0063; P (Vehicle-treated vector vs imatinib-treated vector) = 0.0135; P (Vehicle-treated vector vs the combination therapy-treated vector)

    Article Snippet: The human FGF-2 (DFB50, R & D systems), mouse VEGF (MMV00), and mouse PDGF-BB ELISA assays (MBB00, R & D Systems) were performed according to the manufacturer’s protocol with the standard curve.

    Techniques: Staining, Plasmid Preparation