vegf r2  (Abcam)

 
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    Name:
    Anti VEGF Receptor 2 antibody
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    Catalog Number:
    ab2349
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    Structured Review

    Abcam vegf r2
    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of <t>VEGF-R2</t> signal pathway and disruption of retinal endothelial cell barrier.

    https://www.bioz.com/result/vegf r2/product/Abcam
    Average 99 stars, based on 6 article reviews
    Price from $9.99 to $1999.99
    vegf r2 - by Bioz Stars, 2020-09
    99/100 stars

    Images

    1) Product Images from "12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase"

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057254

    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.
    Figure Legend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Techniques Used: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P
    Figure Legend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Techniques Used: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P
    Figure Legend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Techniques Used: Inhibition, Fluorescence, Permeability

    2) Product Images from "Attenuated PDGF signaling drives alveolar and microvascular defects in neonatal chronic lung disease"

    Article Title: Attenuated PDGF signaling drives alveolar and microvascular defects in neonatal chronic lung disease

    Journal: EMBO Molecular Medicine

    doi: 10.15252/emmm.201607308

    PDGF ‐Rα haploinsufficiency drives reduced pulmonary micro‐vessel density with increased endothelial cell apoptosis in neonatal mice undergoing MV ‐O 2 Histologic and immunoblot analysis displayed reduced small vessel number (20–100 μm diameter) normalized to 100 alveoli as well as reduced pulmonary VEGF‐R2, VE‐cadherin, and VEGF‐A protein levels, respectively ( n = 6–8 mice/group). Panels (B) and (C) are from same blot hence having same β‐actin bands. Immunofluorescence images of lung tissue (400×; merged) from neonatal PDGF‐Rα +/− mice indicating increased cleaved caspase‐3 (red, white arrows; lower panel) after 8 h of MV‐O 2 in contrast to WT mice (upper panel; green: CD31; blue: DAPI). Double stain revealed increased cleaved caspase‐3 + /CD31 + cells normalized to CD31 area in PDGF‐Rα +/− mice after 8 h of MV‐O 2 ( n = 4 mice/group, 4 sections/mice, and 10 images/section). Representative image confirming increased endothelial apoptosis in neonatal PDGF‐Rα +/− mice after 8 h of MV‐O 2 (lower panel; white arrows) with VE‐cadherin (red) and cleaved caspase‐3 (green) and nucleus stained with DAPI (blue) when compared to WT mice (upper panel) ( n = 2 mice/group). Increased caspase‐3 activation in HUVECs upon incubation with supernatants for 6 h obtained from lung mouse myofibroblasts after PDGF‐Rα siRNA treatment when compared to control siRNA ( n = 3 experiments). In vitro application of PDGF‐Rα siRNA to primary lung mouse myofibroblasts from WT mice diminished PDGF‐Rα (H) protein (normalized to control), associated with reduced VEGF‐A protein (I) ( n = 3 mice/group). Increased cleaved caspase‐9 and reduced eNOS protein levels in HUVECs upon incubation with supernatants for 6 h obtained from lung mouse myofibroblasts after PDGF‐Rα siRNA treatment when compared to control siRNA ( n = 3 mice/group). Data information: Data are presented as mean ± SD. *** P
    Figure Legend Snippet: PDGF ‐Rα haploinsufficiency drives reduced pulmonary micro‐vessel density with increased endothelial cell apoptosis in neonatal mice undergoing MV ‐O 2 Histologic and immunoblot analysis displayed reduced small vessel number (20–100 μm diameter) normalized to 100 alveoli as well as reduced pulmonary VEGF‐R2, VE‐cadherin, and VEGF‐A protein levels, respectively ( n = 6–8 mice/group). Panels (B) and (C) are from same blot hence having same β‐actin bands. Immunofluorescence images of lung tissue (400×; merged) from neonatal PDGF‐Rα +/− mice indicating increased cleaved caspase‐3 (red, white arrows; lower panel) after 8 h of MV‐O 2 in contrast to WT mice (upper panel; green: CD31; blue: DAPI). Double stain revealed increased cleaved caspase‐3 + /CD31 + cells normalized to CD31 area in PDGF‐Rα +/− mice after 8 h of MV‐O 2 ( n = 4 mice/group, 4 sections/mice, and 10 images/section). Representative image confirming increased endothelial apoptosis in neonatal PDGF‐Rα +/− mice after 8 h of MV‐O 2 (lower panel; white arrows) with VE‐cadherin (red) and cleaved caspase‐3 (green) and nucleus stained with DAPI (blue) when compared to WT mice (upper panel) ( n = 2 mice/group). Increased caspase‐3 activation in HUVECs upon incubation with supernatants for 6 h obtained from lung mouse myofibroblasts after PDGF‐Rα siRNA treatment when compared to control siRNA ( n = 3 experiments). In vitro application of PDGF‐Rα siRNA to primary lung mouse myofibroblasts from WT mice diminished PDGF‐Rα (H) protein (normalized to control), associated with reduced VEGF‐A protein (I) ( n = 3 mice/group). Increased cleaved caspase‐9 and reduced eNOS protein levels in HUVECs upon incubation with supernatants for 6 h obtained from lung mouse myofibroblasts after PDGF‐Rα siRNA treatment when compared to control siRNA ( n = 3 mice/group). Data information: Data are presented as mean ± SD. *** P

    Techniques Used: Mouse Assay, Immunofluorescence, Staining, Activation Assay, Incubation, In Vitro

    Model for how attenuated PDGF signaling and positive pressure ventilation interact to produce the distinct phenotypic manifestations of nCLD MV‐O 2 in vivo , a combination of O 2 , that is, oxygen and stretch (purple arrow) and/or TGF‐β alone or in combination with mechanical stretch in vitro (yellow arrow), reduces platelet‐derived growth factor receptor α (PDGF‐Rα) levels and its downstream signaling through JAK‐2 and STAT‐3 in the pulmonary myofibroblast (MFB). This reduction in turn abrogates vascular endothelial growth factor expression (VEGF‐A and VEGF‐R2), leading to increased apoptosis in pulmonary endothelial cells (EC). Whereas myofibroblast migration is diminished through reduced RAS and pERK/ERK signaling, stretch alone increases their proliferation, hence depicting the differential effect of the most important denominators of nCLD development in the premature lung undergoing MV‐O 2 . Application of PDGF‐A to premature lung increases PDGF‐Rα levels in an AKT‐dependent manner in turn activating the downstream cascade through JAK‐2, STAT‐3 signaling. This then activates VEGF‐A secretion and VEGF‐R2 activity reducing apoptosis in endothelial cells (ECs).
    Figure Legend Snippet: Model for how attenuated PDGF signaling and positive pressure ventilation interact to produce the distinct phenotypic manifestations of nCLD MV‐O 2 in vivo , a combination of O 2 , that is, oxygen and stretch (purple arrow) and/or TGF‐β alone or in combination with mechanical stretch in vitro (yellow arrow), reduces platelet‐derived growth factor receptor α (PDGF‐Rα) levels and its downstream signaling through JAK‐2 and STAT‐3 in the pulmonary myofibroblast (MFB). This reduction in turn abrogates vascular endothelial growth factor expression (VEGF‐A and VEGF‐R2), leading to increased apoptosis in pulmonary endothelial cells (EC). Whereas myofibroblast migration is diminished through reduced RAS and pERK/ERK signaling, stretch alone increases their proliferation, hence depicting the differential effect of the most important denominators of nCLD development in the premature lung undergoing MV‐O 2 . Application of PDGF‐A to premature lung increases PDGF‐Rα levels in an AKT‐dependent manner in turn activating the downstream cascade through JAK‐2, STAT‐3 signaling. This then activates VEGF‐A secretion and VEGF‐R2 activity reducing apoptosis in endothelial cells (ECs).

    Techniques Used: In Vivo, In Vitro, Derivative Assay, Expressing, Migration, Activity Assay

    3) Product Images from "12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase"

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057254

    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.
    Figure Legend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Techniques Used: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P
    Figure Legend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Techniques Used: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P
    Figure Legend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Techniques Used: Inhibition, Fluorescence, Permeability

    4) Product Images from "12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase"

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057254

    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.
    Figure Legend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Techniques Used: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P
    Figure Legend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Techniques Used: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P
    Figure Legend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Techniques Used: Inhibition, Fluorescence, Permeability

    5) Product Images from "Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model"

    Article Title: Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model

    Journal: OncoTargets and therapy

    doi: 10.2147/OTT.S69830

    Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P
    Figure Legend Snippet: Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P

    Techniques Used: Expressing, Transplantation Assay, Western Blot

    6) Product Images from "Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model"

    Article Title: Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model

    Journal: OncoTargets and therapy

    doi: 10.2147/OTT.S69830

    Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P
    Figure Legend Snippet: Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P

    Techniques Used: Expressing, Transplantation Assay, Western Blot

    7) Product Images from "Cerebral microvascular rarefaction induced by whole brain radiation is reversible by systemic hypoxia in mice"

    Article Title: Cerebral microvascular rarefaction induced by whole brain radiation is reversible by systemic hypoxia in mice

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    doi: 10.1152/ajpheart.01024.2010

    Confirmation of hypoxic status of animals. Hematocrit ( A ) and vascular endothelial growth factor (VEGF, B ) protein levels increased in response to hypoxia treatment in both groups ( n = 8–16 animals/group). C : representative Western blot for VEGF receptor (R) 2 levels. D : quantification of Western blot analysis showed that VEGF-R2 protein levels increased in the control animals in response to hypoxia and also increased in response to radiation ( n = 6/group). E : representative Western blot for cortical hypoxia-inducible factor (HIF)-1α in nuclear fractions. F : quantification of the Western blot showed that, in the normoxic-treated radiated group, nuclear HIF-1α is increased compared with controls ( n = 4/group). CN, control normoxia; CH, control hypoxia; RN, radiated normoxia; RH, radiated hypoxia. * P
    Figure Legend Snippet: Confirmation of hypoxic status of animals. Hematocrit ( A ) and vascular endothelial growth factor (VEGF, B ) protein levels increased in response to hypoxia treatment in both groups ( n = 8–16 animals/group). C : representative Western blot for VEGF receptor (R) 2 levels. D : quantification of Western blot analysis showed that VEGF-R2 protein levels increased in the control animals in response to hypoxia and also increased in response to radiation ( n = 6/group). E : representative Western blot for cortical hypoxia-inducible factor (HIF)-1α in nuclear fractions. F : quantification of the Western blot showed that, in the normoxic-treated radiated group, nuclear HIF-1α is increased compared with controls ( n = 4/group). CN, control normoxia; CH, control hypoxia; RN, radiated normoxia; RH, radiated hypoxia. * P

    Techniques Used: Western Blot

    8) Product Images from "Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model"

    Article Title: Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model

    Journal: OncoTargets and therapy

    doi: 10.2147/OTT.S69830

    Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P
    Figure Legend Snippet: Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P

    Techniques Used: Expressing, Transplantation Assay, Western Blot

    9) Product Images from "12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase"

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057254

    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.
    Figure Legend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Techniques Used: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P
    Figure Legend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Techniques Used: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P
    Figure Legend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Techniques Used: Inhibition, Fluorescence, Permeability

    10) Product Images from "12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase"

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057254

    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.
    Figure Legend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Techniques Used: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P
    Figure Legend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Techniques Used: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P
    Figure Legend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Techniques Used: Inhibition, Fluorescence, Permeability

    11) Product Images from "12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase"

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057254

    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.
    Figure Legend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Techniques Used: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P
    Figure Legend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Techniques Used: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P
    Figure Legend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Techniques Used: Inhibition, Fluorescence, Permeability

    12) Product Images from "Sublethal total body irradiation leads to early cerebellar damage and oxidative stress"

    Article Title: Sublethal total body irradiation leads to early cerebellar damage and oxidative stress

    Journal: Current neurovascular research

    doi:

    VEGF-R2 and 8-OHdG immunoreactivities in the microvessel endothelial cells after TBI. The VEGF-R2 or the 8-OHdG was rarely detectable in 0 day (A). The VEGF-R2 were found to be co-localized with the 8-OHdG in the microvessel endothelial cells 1 day after TBI (B). The co-localization of the VEGF-R2 and 8-OHdG immunoreactivities was further verified in the high magnification image (C). Arrows indicate endothelial cells which stain yellow after merging the VEGF-R2 labeling color (green, image (D)), and the 8-OHdG labeling color (red, image (E)).
    Figure Legend Snippet: VEGF-R2 and 8-OHdG immunoreactivities in the microvessel endothelial cells after TBI. The VEGF-R2 or the 8-OHdG was rarely detectable in 0 day (A). The VEGF-R2 were found to be co-localized with the 8-OHdG in the microvessel endothelial cells 1 day after TBI (B). The co-localization of the VEGF-R2 and 8-OHdG immunoreactivities was further verified in the high magnification image (C). Arrows indicate endothelial cells which stain yellow after merging the VEGF-R2 labeling color (green, image (D)), and the 8-OHdG labeling color (red, image (E)).

    Techniques Used: Staining, Labeling

    13) Product Images from "Generation of Human Epidermis-Derived Mesenchymal Stem Cell-like Pluripotent Cells (hEMSCPCs)"

    Article Title: Generation of Human Epidermis-Derived Mesenchymal Stem Cell-like Pluripotent Cells (hEMSCPCs)

    Journal: Scientific Reports

    doi: 10.1038/srep01933

    Immunohistochemical expression patterns of hEMSCPCs over 30 passages. (A): Some cells at P2 showed nestin positive immunoreactivity (brown color). (B): Almost all cells at P2 were vimentin positive (brown color). (C): Almost all cells at P10, P20, and P30 showed nestin immunoreactivity (brown color). (D): Almost all cells at P10, P20, and P30 were vimentin immunoreactive (brown color). (E): At P2, P10, P20, and P30, a small number of cells were CK19 immunoreactive (brown color). (F): At P2, P10, P20, and P30, a limited number of CD10 immunoreactive cells were observed (brown color). (G): At P2, P10, P20, and P30, a few individual cells were CD3 immunoreactive (brown color). (H): At P2, no CD31-positive or VEGF R2-positive cells were seen. (I): At P10, P20, and P30, almost all cells expressed CD90 (green fluorescence). (J): At P2, P10, P20, and P30, most cells expressed CD73 (green fluorescence). (K): At P2, P10, P20, and P30, a fraction of cells expressed CD105 (green fluorescence). (L): At P10, P20, and P30, some specimens had no HLA-DR-positive cells. (M): At P10, P20, and P30, a small number of HLA-I-positive cells were observed in some specimens (green fluorescence).
    Figure Legend Snippet: Immunohistochemical expression patterns of hEMSCPCs over 30 passages. (A): Some cells at P2 showed nestin positive immunoreactivity (brown color). (B): Almost all cells at P2 were vimentin positive (brown color). (C): Almost all cells at P10, P20, and P30 showed nestin immunoreactivity (brown color). (D): Almost all cells at P10, P20, and P30 were vimentin immunoreactive (brown color). (E): At P2, P10, P20, and P30, a small number of cells were CK19 immunoreactive (brown color). (F): At P2, P10, P20, and P30, a limited number of CD10 immunoreactive cells were observed (brown color). (G): At P2, P10, P20, and P30, a few individual cells were CD3 immunoreactive (brown color). (H): At P2, no CD31-positive or VEGF R2-positive cells were seen. (I): At P10, P20, and P30, almost all cells expressed CD90 (green fluorescence). (J): At P2, P10, P20, and P30, most cells expressed CD73 (green fluorescence). (K): At P2, P10, P20, and P30, a fraction of cells expressed CD105 (green fluorescence). (L): At P10, P20, and P30, some specimens had no HLA-DR-positive cells. (M): At P10, P20, and P30, a small number of HLA-I-positive cells were observed in some specimens (green fluorescence).

    Techniques Used: Immunohistochemistry, Expressing, Fluorescence

    Flow cytometry analysis of cell marker expression over time in culture. Flow cytometry plots for various markers at P2, P10, P20, and P30. (A): CD73 was always highly expressed at P2, P10, P20, and P30; CD90 was moderately expressed at P2, and highly expressed at P10, P20, and P30; CD105 was moderately expressed at P2, P10, P20 and P30. (B): Substantial vimentin expression was observed at P2, P10, P20, and P30. Nestin expression mirrored CD90 expression. Ne stin expression was moderate at P2 but high at P10, P20, and P30, whereas GFAP and β-III tubulin showed minimal expression throughout the culture period. (C): Human EMSCPCs expressed very low levels of CD34, CD45, CD3, CD19 and CD16. (D): CD10 expression was always low, while CK19, CD31, and VEGF R2 were barely detectable. (E): The tissue compatibility antigens HLA-DR and HLA-I were moderately or minimally expressed at P2; with increasing number of passages, fewer and fewer cells expressed these markers. No HLA-DR-positive cells were detected in some specimens at P10, P20, and P30.
    Figure Legend Snippet: Flow cytometry analysis of cell marker expression over time in culture. Flow cytometry plots for various markers at P2, P10, P20, and P30. (A): CD73 was always highly expressed at P2, P10, P20, and P30; CD90 was moderately expressed at P2, and highly expressed at P10, P20, and P30; CD105 was moderately expressed at P2, P10, P20 and P30. (B): Substantial vimentin expression was observed at P2, P10, P20, and P30. Nestin expression mirrored CD90 expression. Ne stin expression was moderate at P2 but high at P10, P20, and P30, whereas GFAP and β-III tubulin showed minimal expression throughout the culture period. (C): Human EMSCPCs expressed very low levels of CD34, CD45, CD3, CD19 and CD16. (D): CD10 expression was always low, while CK19, CD31, and VEGF R2 were barely detectable. (E): The tissue compatibility antigens HLA-DR and HLA-I were moderately or minimally expressed at P2; with increasing number of passages, fewer and fewer cells expressed these markers. No HLA-DR-positive cells were detected in some specimens at P10, P20, and P30.

    Techniques Used: Flow Cytometry, Cytometry, Marker, Expressing

    14) Product Images from "12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase"

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057254

    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.
    Figure Legend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Techniques Used: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P
    Figure Legend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Techniques Used: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P
    Figure Legend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Techniques Used: Inhibition, Fluorescence, Permeability

    15) Product Images from "12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase"

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057254

    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.
    Figure Legend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Techniques Used: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P
    Figure Legend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Techniques Used: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P
    Figure Legend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Techniques Used: Inhibition, Fluorescence, Permeability

    16) Product Images from "Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model"

    Article Title: Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model

    Journal: OncoTargets and therapy

    doi: 10.2147/OTT.S69830

    Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P
    Figure Legend Snippet: Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P

    Techniques Used: Expressing, Transplantation Assay, Western Blot

    17) Product Images from "Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model"

    Article Title: Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model

    Journal: OncoTargets and therapy

    doi: 10.2147/OTT.S69830

    Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P
    Figure Legend Snippet: Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P

    Techniques Used: Expressing, Transplantation Assay, Western Blot

    18) Product Images from "Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model"

    Article Title: Ginsenoside Rg3 attenuates hepatoma VEGF overexpression after hepatic artery embolization in an orthotopic transplantation hepatocellular carcinoma rat model

    Journal: OncoTargets and therapy

    doi: 10.2147/OTT.S69830

    Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P
    Figure Legend Snippet: Ginsenoside Rg3 reduced hepatoma VEGF-R2 expression and phosphorylation after TAE in an orthotopic transplantation HCC rat model. Notes: ( A ) VEGF-R2 expression and phosphorylation were determined by Western blot. Protein expression was normalized to GAPDH. The data represent the mean ± SD of three independent experiments. * P

    Techniques Used: Expressing, Transplantation Assay, Western Blot

    19) Product Images from "12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase"

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057254

    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.
    Figure Legend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Techniques Used: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P
    Figure Legend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Techniques Used: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P
    Figure Legend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Techniques Used: Inhibition, Fluorescence, Permeability

    20) Product Images from "12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase"

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057254

    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.
    Figure Legend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Techniques Used: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P
    Figure Legend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Techniques Used: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P
    Figure Legend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Techniques Used: Inhibition, Fluorescence, Permeability

    Related Articles

    Immunohistochemistry:

    Article Title: Effects of ischemic postconditioning on neuronal VEGF regulation and microglial polarization in a rat model of focal cerebral ischemia
    Article Snippet: .. Immunohistochemistry was performed on 6 sham, 6 MCAO, 5 postconditioning and 5 postconditioning plus FLK-1 inhibitor rats, using primary antibodies anti-VEGF (1:500, Santa Cruz Biotechnology, Cat# sc-152, RRID:AB_2212984) and anti-VEGFR2 (1:200, Abcam, Cat# ab45010, RRID:AB_883436); anti-GFAP (1:200, Invitrogen, Scientific Cat# 13-0300, RRID:AB_2532994) as a marker of activated astrocytes; anti-Iba1 (1:200, Wako, Cat# 019-19471, RRID:AB_2665520) as marker of microglia; anti-CD68 (1:100, Abcam, Cat# ab955, RRID:AB_307338) as a general microglia activation marker; anti-CD206 (1:200, Santa Cruz Biotechnology, Cat# sc-34577, RRID:AB_2144904) as an M2-like marker; anti-CD86 (1:200, Abcam, Cat# ab53004, RRID:AB_869050) as an M1-like marker, and anti-NeuN (1:100, Millipore, Cat# MAB377, RRID:AB_2298772) as a marker of neurons. .. To investigate increase in angiogenesis, immunostaining was performed by quantifying microvessels that were double-positive for collagen-IV (1:10, SouthernBiotech) for vascular remodeling and Ki67 (1:500, Abcam, Cat# ab16667, RRID:AB_302459) a general cell proliferation marker.

    Blocking Assay:

    Article Title: Morphological Plasticity of Emerging Purkinje Cells in Response to Exogenous VEGF
    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. .. After washing with PBS, secondary FITC-coupled anti-rabbit IgG (goat, 1:400, F6005; Sigma Aldrich) or Alexa Fluor 488-coupled anti-rabbit IgG (goat, 1:400, A-11008, Molecular Probes) antibodies were added overnight at 4°C.

    Activation Assay:

    Article Title: Effects of ischemic postconditioning on neuronal VEGF regulation and microglial polarization in a rat model of focal cerebral ischemia
    Article Snippet: .. Immunohistochemistry was performed on 6 sham, 6 MCAO, 5 postconditioning and 5 postconditioning plus FLK-1 inhibitor rats, using primary antibodies anti-VEGF (1:500, Santa Cruz Biotechnology, Cat# sc-152, RRID:AB_2212984) and anti-VEGFR2 (1:200, Abcam, Cat# ab45010, RRID:AB_883436); anti-GFAP (1:200, Invitrogen, Scientific Cat# 13-0300, RRID:AB_2532994) as a marker of activated astrocytes; anti-Iba1 (1:200, Wako, Cat# 019-19471, RRID:AB_2665520) as marker of microglia; anti-CD68 (1:100, Abcam, Cat# ab955, RRID:AB_307338) as a general microglia activation marker; anti-CD206 (1:200, Santa Cruz Biotechnology, Cat# sc-34577, RRID:AB_2144904) as an M2-like marker; anti-CD86 (1:200, Abcam, Cat# ab53004, RRID:AB_869050) as an M1-like marker, and anti-NeuN (1:100, Millipore, Cat# MAB377, RRID:AB_2298772) as a marker of neurons. .. To investigate increase in angiogenesis, immunostaining was performed by quantifying microvessels that were double-positive for collagen-IV (1:10, SouthernBiotech) for vascular remodeling and Ki67 (1:500, Abcam, Cat# ab16667, RRID:AB_302459) a general cell proliferation marker.

    Incubation:

    Article Title: Morphological Plasticity of Emerging Purkinje Cells in Response to Exogenous VEGF
    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. .. After washing with PBS, secondary FITC-coupled anti-rabbit IgG (goat, 1:400, F6005; Sigma Aldrich) or Alexa Fluor 488-coupled anti-rabbit IgG (goat, 1:400, A-11008, Molecular Probes) antibodies were added overnight at 4°C.

    Article Title: Apatinib affect VEGF-mediated cell proliferation, migration, invasion via blocking VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways in cholangiocarcinoma cell
    Article Snippet: .. The membrane was then blocked with 5% milk diluted in PBS at room temperature for 1 h, followed by incubated with 1:1000 VEGFR2 antibody (ab10972, Abcam, Cambridge, MA, USA),1:5000 p-VEGFR2 (ab38473, Abcam), 1:2000 p-MEK (2338, CST), 1:1000 MEK (4694, CST), 1:2000 p-ERK1/2 (4370, CST), 1:1000 ERK (4695, CST), 1:2000 slug (ab51772, Abcam), 1:3000 Snail (ab53519, Abcam), 1:2500 MMP9 (ab38898, Abcam), 1:1500 P-AKT (ab81283, Abcam), 1:1500 AKT (ab179463, Abcam) and 1:5000 GAPDH antibody (ab8245, Abcam) overnight at 4 °C separately. .. Once primary antibodies were washed, membrane was incubated with goat anti-rabbit horseradish peroxidase-labeled secondary antibody (Sangon Biotech, Shanghai, China).

    Article Title: Platelet-derived growth factor D promotes the angiogenic capacity of endothelial progenitor cells
    Article Snippet: .. Briefly, cells were incubated with primary antibodies against CD133 (Ab2839; Abcam, Cambridge, MA, USA) at a dilution of 1:150, VEGFR2 (Ab2349; Abcam) at a dilution of 1:200 and CD34 (ab2839; Abcam) at a dilution of 1:150, FITC-UEA-lectin (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany) at a dilution of 1:150 and Dil-AcLDL (Biomedical Technologies, Madrid, Spain) at a dilution of 1:150, followed by incubation with anti-Alexa Fluor 647-FITC (Cwbiotech, Beijing, China) secondary antibody at a dilution of 1:200 as referred to our previous research ( ). .. Then, cells were counterstained with DAPI (Roche Diagnostics, Basel, Switzerland) and imaged with a fluorescence microscope.

    Article Title: Oxidative Stress Induces a VEGF Autocrine Loop in the Retina: Relevance for Diabetic Retinopathy
    Article Snippet: .. Then, the cells were incubated overnight at 4 °C with an anti-VEGFR2 antibody (ab2349, Abcam, Cambridge, UK; 1:400 dilution) or with an anti-Nrf2 antibody (ab62352, Abcam; 1:500 dilution) and successively with an anti-rabbit secondary antibody conjugated with Alexa-Fluor-488 (Life Technologies, Carlsbad, CA, USA, 1:200 dilution) or with an anti-rabbit secondary antibody conjugated with Cy3 (Sigma-Aldrich, 1:200 dilution) for 1 h at room temperature. .. After staining of the nuclei with Hoechst 33242 dye (40,6-diamidino-2-phenylindole; ThermoFisher Scientific) and actin filaments with rhodamine-conjugated phalloidin (ThermoFisher Scientific) to visualize cell shape, the cells were dried and mounted with ProLong Diamond Antifade Mountant (Thermo Fisher Scientific).

    Migration:

    Article Title: Vascular endothelial growth factor participates in modulating the C6 glioma-induced migration of rat bone marrow-derived mesenchymal stem cells and upregulates their vascular cell adhesion molecule-1 expression
    Article Snippet: .. Moreover, to ascertain whether VEGF promotes the migration of BMSCs towards C6 glioma, we examined the migration of BMSCs in response to a suspension of C6 glioma cells supplemented with or without a VEGF neutralizing antibody (1 μ g/ml, Abcam, Cambridge, UK), which were placed in the lower chambers, respectively. ..

    Marker:

    Article Title: Effects of ischemic postconditioning on neuronal VEGF regulation and microglial polarization in a rat model of focal cerebral ischemia
    Article Snippet: .. Immunohistochemistry was performed on 6 sham, 6 MCAO, 5 postconditioning and 5 postconditioning plus FLK-1 inhibitor rats, using primary antibodies anti-VEGF (1:500, Santa Cruz Biotechnology, Cat# sc-152, RRID:AB_2212984) and anti-VEGFR2 (1:200, Abcam, Cat# ab45010, RRID:AB_883436); anti-GFAP (1:200, Invitrogen, Scientific Cat# 13-0300, RRID:AB_2532994) as a marker of activated astrocytes; anti-Iba1 (1:200, Wako, Cat# 019-19471, RRID:AB_2665520) as marker of microglia; anti-CD68 (1:100, Abcam, Cat# ab955, RRID:AB_307338) as a general microglia activation marker; anti-CD206 (1:200, Santa Cruz Biotechnology, Cat# sc-34577, RRID:AB_2144904) as an M2-like marker; anti-CD86 (1:200, Abcam, Cat# ab53004, RRID:AB_869050) as an M1-like marker, and anti-NeuN (1:100, Millipore, Cat# MAB377, RRID:AB_2298772) as a marker of neurons. .. To investigate increase in angiogenesis, immunostaining was performed by quantifying microvessels that were double-positive for collagen-IV (1:10, SouthernBiotech) for vascular remodeling and Ki67 (1:500, Abcam, Cat# ab16667, RRID:AB_302459) a general cell proliferation marker.

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    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of <t>VEGF-R2</t> signal pathway and disruption of retinal endothelial cell barrier.
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    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Journal: PLoS ONE

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    doi: 10.1371/journal.pone.0057254

    Figure Lengend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Article Snippet: In particular, NADPH oxidase has been shown to modulate VEGF signaling pathway in endothelial cells via activating VEGF-R2 , .

    Techniques: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Journal: PLoS ONE

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    doi: 10.1371/journal.pone.0057254

    Figure Lengend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Article Snippet: In particular, NADPH oxidase has been shown to modulate VEGF signaling pathway in endothelial cells via activating VEGF-R2 , .

    Techniques: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Journal: PLoS ONE

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    doi: 10.1371/journal.pone.0057254

    Figure Lengend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Article Snippet: In particular, NADPH oxidase has been shown to modulate VEGF signaling pathway in endothelial cells via activating VEGF-R2 , .

    Techniques: Inhibition, Fluorescence, Permeability

    PDGF ‐Rα haploinsufficiency drives reduced pulmonary micro‐vessel density with increased endothelial cell apoptosis in neonatal mice undergoing MV ‐O 2 Histologic and immunoblot analysis displayed reduced small vessel number (20–100 μm diameter) normalized to 100 alveoli as well as reduced pulmonary VEGF‐R2, VE‐cadherin, and VEGF‐A protein levels, respectively ( n = 6–8 mice/group). Panels (B) and (C) are from same blot hence having same β‐actin bands. Immunofluorescence images of lung tissue (400×; merged) from neonatal PDGF‐Rα +/− mice indicating increased cleaved caspase‐3 (red, white arrows; lower panel) after 8 h of MV‐O 2 in contrast to WT mice (upper panel; green: CD31; blue: DAPI). Double stain revealed increased cleaved caspase‐3 + /CD31 + cells normalized to CD31 area in PDGF‐Rα +/− mice after 8 h of MV‐O 2 ( n = 4 mice/group, 4 sections/mice, and 10 images/section). Representative image confirming increased endothelial apoptosis in neonatal PDGF‐Rα +/− mice after 8 h of MV‐O 2 (lower panel; white arrows) with VE‐cadherin (red) and cleaved caspase‐3 (green) and nucleus stained with DAPI (blue) when compared to WT mice (upper panel) ( n = 2 mice/group). Increased caspase‐3 activation in HUVECs upon incubation with supernatants for 6 h obtained from lung mouse myofibroblasts after PDGF‐Rα siRNA treatment when compared to control siRNA ( n = 3 experiments). In vitro application of PDGF‐Rα siRNA to primary lung mouse myofibroblasts from WT mice diminished PDGF‐Rα (H) protein (normalized to control), associated with reduced VEGF‐A protein (I) ( n = 3 mice/group). Increased cleaved caspase‐9 and reduced eNOS protein levels in HUVECs upon incubation with supernatants for 6 h obtained from lung mouse myofibroblasts after PDGF‐Rα siRNA treatment when compared to control siRNA ( n = 3 mice/group). Data information: Data are presented as mean ± SD. *** P

    Journal: EMBO Molecular Medicine

    Article Title: Attenuated PDGF signaling drives alveolar and microvascular defects in neonatal chronic lung disease

    doi: 10.15252/emmm.201607308

    Figure Lengend Snippet: PDGF ‐Rα haploinsufficiency drives reduced pulmonary micro‐vessel density with increased endothelial cell apoptosis in neonatal mice undergoing MV ‐O 2 Histologic and immunoblot analysis displayed reduced small vessel number (20–100 μm diameter) normalized to 100 alveoli as well as reduced pulmonary VEGF‐R2, VE‐cadherin, and VEGF‐A protein levels, respectively ( n = 6–8 mice/group). Panels (B) and (C) are from same blot hence having same β‐actin bands. Immunofluorescence images of lung tissue (400×; merged) from neonatal PDGF‐Rα +/− mice indicating increased cleaved caspase‐3 (red, white arrows; lower panel) after 8 h of MV‐O 2 in contrast to WT mice (upper panel; green: CD31; blue: DAPI). Double stain revealed increased cleaved caspase‐3 + /CD31 + cells normalized to CD31 area in PDGF‐Rα +/− mice after 8 h of MV‐O 2 ( n = 4 mice/group, 4 sections/mice, and 10 images/section). Representative image confirming increased endothelial apoptosis in neonatal PDGF‐Rα +/− mice after 8 h of MV‐O 2 (lower panel; white arrows) with VE‐cadherin (red) and cleaved caspase‐3 (green) and nucleus stained with DAPI (blue) when compared to WT mice (upper panel) ( n = 2 mice/group). Increased caspase‐3 activation in HUVECs upon incubation with supernatants for 6 h obtained from lung mouse myofibroblasts after PDGF‐Rα siRNA treatment when compared to control siRNA ( n = 3 experiments). In vitro application of PDGF‐Rα siRNA to primary lung mouse myofibroblasts from WT mice diminished PDGF‐Rα (H) protein (normalized to control), associated with reduced VEGF‐A protein (I) ( n = 3 mice/group). Increased cleaved caspase‐9 and reduced eNOS protein levels in HUVECs upon incubation with supernatants for 6 h obtained from lung mouse myofibroblasts after PDGF‐Rα siRNA treatment when compared to control siRNA ( n = 3 mice/group). Data information: Data are presented as mean ± SD. *** P

    Article Snippet: After measurement of protein concentrations (BCA, #23227, Pierce Scientific), immunoblots were performed using a Bis‐Tris or a Tris‐Acetate gel (#NP0321BOX, #EA0375BOX, Life Technologies) using the following antibodies: PDGF‐Rα (C‐20, Santa Cruz Biotechnology #338), VEGF‐A (147, Santa Cruz Biotechnology #507), VEGF‐R2 (Abcam, Cambridge, USA #Ab2349), VE‐cadherin (H‐72, Santa Cruz Biotechnology #28644), cleaved caspase‐3 (Cell Signaling Technology #9661), cleaved caspase‐9 (Cell Signaling Technologies #7237), eNOS (Cell Signaling Technologies #5880), phospho‐ERK (Cell Signaling Technologies #4370), total ERK (Cell Signaling Technologies #4695), RAS (Cell Signaling Technologies #8955), PI3K (Cell Signaling Technologies #13666), JAK‐2 (Cell Signaling Technologies #3230), STAT‐3 (Cell Signaling Technologies #9139).

    Techniques: Mouse Assay, Immunofluorescence, Staining, Activation Assay, Incubation, In Vitro

    Model for how attenuated PDGF signaling and positive pressure ventilation interact to produce the distinct phenotypic manifestations of nCLD MV‐O 2 in vivo , a combination of O 2 , that is, oxygen and stretch (purple arrow) and/or TGF‐β alone or in combination with mechanical stretch in vitro (yellow arrow), reduces platelet‐derived growth factor receptor α (PDGF‐Rα) levels and its downstream signaling through JAK‐2 and STAT‐3 in the pulmonary myofibroblast (MFB). This reduction in turn abrogates vascular endothelial growth factor expression (VEGF‐A and VEGF‐R2), leading to increased apoptosis in pulmonary endothelial cells (EC). Whereas myofibroblast migration is diminished through reduced RAS and pERK/ERK signaling, stretch alone increases their proliferation, hence depicting the differential effect of the most important denominators of nCLD development in the premature lung undergoing MV‐O 2 . Application of PDGF‐A to premature lung increases PDGF‐Rα levels in an AKT‐dependent manner in turn activating the downstream cascade through JAK‐2, STAT‐3 signaling. This then activates VEGF‐A secretion and VEGF‐R2 activity reducing apoptosis in endothelial cells (ECs).

    Journal: EMBO Molecular Medicine

    Article Title: Attenuated PDGF signaling drives alveolar and microvascular defects in neonatal chronic lung disease

    doi: 10.15252/emmm.201607308

    Figure Lengend Snippet: Model for how attenuated PDGF signaling and positive pressure ventilation interact to produce the distinct phenotypic manifestations of nCLD MV‐O 2 in vivo , a combination of O 2 , that is, oxygen and stretch (purple arrow) and/or TGF‐β alone or in combination with mechanical stretch in vitro (yellow arrow), reduces platelet‐derived growth factor receptor α (PDGF‐Rα) levels and its downstream signaling through JAK‐2 and STAT‐3 in the pulmonary myofibroblast (MFB). This reduction in turn abrogates vascular endothelial growth factor expression (VEGF‐A and VEGF‐R2), leading to increased apoptosis in pulmonary endothelial cells (EC). Whereas myofibroblast migration is diminished through reduced RAS and pERK/ERK signaling, stretch alone increases their proliferation, hence depicting the differential effect of the most important denominators of nCLD development in the premature lung undergoing MV‐O 2 . Application of PDGF‐A to premature lung increases PDGF‐Rα levels in an AKT‐dependent manner in turn activating the downstream cascade through JAK‐2, STAT‐3 signaling. This then activates VEGF‐A secretion and VEGF‐R2 activity reducing apoptosis in endothelial cells (ECs).

    Article Snippet: After measurement of protein concentrations (BCA, #23227, Pierce Scientific), immunoblots were performed using a Bis‐Tris or a Tris‐Acetate gel (#NP0321BOX, #EA0375BOX, Life Technologies) using the following antibodies: PDGF‐Rα (C‐20, Santa Cruz Biotechnology #338), VEGF‐A (147, Santa Cruz Biotechnology #507), VEGF‐R2 (Abcam, Cambridge, USA #Ab2349), VE‐cadherin (H‐72, Santa Cruz Biotechnology #28644), cleaved caspase‐3 (Cell Signaling Technology #9661), cleaved caspase‐9 (Cell Signaling Technologies #7237), eNOS (Cell Signaling Technologies #5880), phospho‐ERK (Cell Signaling Technologies #4370), total ERK (Cell Signaling Technologies #4695), RAS (Cell Signaling Technologies #8955), PI3K (Cell Signaling Technologies #13666), JAK‐2 (Cell Signaling Technologies #3230), STAT‐3 (Cell Signaling Technologies #9139).

    Techniques: In Vivo, In Vitro, Derivative Assay, Expressing, Migration, Activity Assay