Roles of reactive oxygen species in angiopoietin‐1/tie‐2 receptor signaling

Harfouche, Rania; Malak, Nelly Abdel; Brandes, Ralf P.; Karsan, Aly; Irani, Kaikobad; Hussain, Sabah N. A.

doi:10.1096/fj.04-3621fje

Cited by 116 publications

(112 citation statements)

References 54 publications

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“…These data contrast with those of Wu et al (78) who showed that VEGF-mediated phosphorylation of JNK was oxidasedependent. Moreover, previous studies in HUVEC have demonstrated a role for ROS in VEGF-mediated activation of ERK1/2 in HUVEC and porcine aortic endothelial cells (23,36). The reason for the discrepancies between these latter reports and the present study is not clear.…”

Section: Discussioncontrasting

confidence: 99%

“…Chen et al (35) demonstrated that Ang1-dependent phosphorylation of Akt at Ser-473 in porcine and murine endothelial cells was dependent on NADPH oxidase-derived ROS. In another study, Ang1-mediated phosphorylation of Akt in HUVEC was unaffected by overexpression of superoxide dismutase, catalase, or dominant-negative Rac1 (Rac1N17) (36). We have found that hepatocyte growth factor-mediated activation of Akt in HCAEC occurs independently of NADPH oxidase activity (supplemental Fig.…”

Section: Discussionmentioning

confidence: 76%

“…Many different agonists have been shown to induce endothelial NADPH oxidase activity, including hemodynamic forces (32)(33)(34), VEGF (21,22,24), angiopoietin-1 (Ang1) (21,35,36), tumor necrosis factor-␣ (37), thrombin (38), angiotensin II (37,39), endothelin-1 (40), transforming growth factor-␤ (41), oxidized low density lipoprotein (27), and high potassium (42). Activation of NADPH oxidase is mediated by post-translational modification and/or increased transcription of the regulatory subunits.…”

Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 99%

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NADPH Oxidase Activity Selectively Modulates Vascular Endothelial Growth Factor Signaling Pathways

Abid¹,

Spokes²,

Shih

et al. 2007

Journal of Biological Chemistry

138

125

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Vascular endothelial growth factor (VEGF) and reactive oxygen species (ROS) play critical roles in vascular physiology and pathophysiology. We have demonstrated previously that NADPH oxidase-derived ROS are required for VEGF-mediated migration and proliferation of endothelial cells. The goal of this study was to determine the extent to which VEGF signaling is coupled to NADPH oxidase activity. Human umbilical vein endothelial cells and/or human coronary artery endothelial cells were transfected with short interfering RNA against the p47 phox subunit of NADPH oxidase, treated in the absence or presence of VEGF, and assayed for signaling, gene expression, and function. We show that NADPH oxidase activity is required for VEGF activation of phosphoinositide 3-kinase-Akt-forkhead, and p38 MAPK, but not ERK1/2 or JNK. The permissive role of NADPH oxidase on phosphoinositide 3-kinase-Akt-forkhead signaling is mediated at post-VEGF receptor levels and involves the nonreceptor tyrosine kinase Src. DNA microarrays revealed the existence of two distinct classes of VEGF-responsive genes, one that is ROS-dependent and another that is independent of ROS levels. VEGF-induced, thrombomodulin-dependent activation of protein C was dependent on NADPH oxidase activity, whereas VEGF-induced decay-accelerating factor-mediated protection of endothelial cells against complement-mediated lysis was not. Taken together, these findings suggest that NADPH oxidase-derived ROS selectively modulate some but not all the effects of VEGF on endothelial cell phenotypes.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 76%

Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 99%

See 1 more Smart Citation

NADPH Oxidase Activity Selectively Modulates Vascular Endothelial Growth Factor Signaling Pathways

Abid¹,

Spokes²,

Shih

et al. 2007

Journal of Biological Chemistry

138

125

View full text Add to dashboard Cite

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“…Accumulating evidence suggests that high levels of ROS could act as signaling molecules to mediate various growth-related responses, including angiogenesis. It has been reported that VEGF (vascular endothelial growth factor) and angiopoietin-1 (Ang1), two angiogenic growth factors, induce EC migration through an increase in ROS [13,26] . Recently, Zhao et al reported that ROS promote the formation of new vessels in the infracted heart and contribute to cardiac repair [25] .…”

Section: Discussionmentioning

confidence: 99%

N-benzyl-5-phenyl-1H-pyrazole-3-carboxamide promotes vascular endothelial cell angiogenesis and migration in the absence of serum and FGF-2

Zhang

Huang

et al. 2011

Acta Pharmacol Sin

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Aim: To investigate the effect of N-benzyl-5-phenyl-1H-pyrazole-3-carboxamide (BPC) on angiogenesis in human umbilical vein endothelial cells (HUVECs).Methods: Capillary-like tube formation on matrigel and cell migration analyses were performed in the absence of serum and fibroblast growth factor (FGF-2). Reactive oxygen species (ROS) were measured using a fluorescent probe, 2', 7'-dichlorodihydrofluorescein (DCHF). The nitric oxide (NO) production of HUVECs was examined using a NO detection kit. Morphological observation under a phase contrast microscope, a viability assay using 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl-tetrazolium (MTT) and a lactate dehydrogenase (LDH) activity analysis by a detection kit were performed to evaluate the toxicity of BPC on HUVECs in the presence of serum and FGF-2. The level of hypoxia-inducible factor 1α (HIF-1α) and the release of vascular endothelial growth factor (VEGF) were measured by Western blot and ELISA, respectively. Results: In the absence of serum and FGF-2, cells treated with BPC (5-20 μmol/L) rapidly aligned with one another and formed tubelike structures within 12 h. In the presence of serum and FGF-2, cells treated with BPC for 24, 48 and 72 h had no changes in morphology, viability or LDH release compared with the control group. Cell migration in the BPC-treated group was significantly increased compared with the control group. During this process, NO production and ROS level were elevated dramatically, and the levels of HIF-1α and VEGF were increased dependent on the generation of ROS. Conclusion: BPC most effectively promoted angiogenesis and migration in HUVECs in the absence of FGF-2 and serum.

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“…ROS may play a role as the mediator for the consequence of tumor induced the expression of tumor biomarkers involved tumor angiogenesis. The activation for VEGF and angiopoietin-1 induced EC migration and/or proliferation through an increase in ROS mainly proposed by a number of researchers [28,29] . It was found that ethanol stimulated actin cytoskeletal reorganization, cell motility and tube formation in a ROS-dependent manner in ECs [30] .…”

Section: Discussionmentioning

confidence: 99%

Anti-cancer and anti-angiogenic effects of curcumin and tetrahydrocurcumin on implanted hepatocellular carcinoma in nude mice

Yoysungnoen¹,

Wirachwong²,

Changtam³

et al. 2008

WJG

136

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P < 0.001). Treatment with CUR and THC resulted in significant decrease in the CV (P < 0.005 and P < 0.001, respectively). In particular, the anti-angiogenic effects of CUR and THC were dose-dependent manner. However, the beneficial effect of THC treatment than CUR was observed, in particular, from the 21 d CV (44.96% and 52.86%, P < 0.05). CONCLUSION:THC expressed its anti-angiogenesis without any cytotoxic activities to HepG2 cells even at the highest doses. It is suggested that anti-angiogenic properties of CUR and THC represent a common potential mechanism for their anti-cancer actions. INTRODUCTIONHepatocellular carcinoma (HCC) is a highly malignant tumor characterized by active neovascularization [1] . Since HCC recruit new blood vessels to support tumor growth, an anti-angiogenic agent is one of the goal drugs to treatment of HCC. Cancer cells have a very high rate of mutation in contrast to endothelial cells, which are the main components of blood vessels and have a lower rate of mutation. Because of this genetic stability, anti-cancer treatmenting tumor-induced angiogenesis is expected to be less vulnerable to such drug tolerance. Moreover, it may work on a broad spectrum of solid tumors because all these tumors need to induce angiogenesis for their processes. It is of great interest to apply the idea of antiangiogenesis treatment to the prevention of cancer. If METHODS:T h e 3 -( 4, 5 -d i m e t hy l t h i a zo l -2 -y l ) -2 , 5-diphenyl-tetrazolium bromide (MTT) assay was used for testing the anti-proliferating activities of CUR and THC. In male BALB/c nude mice, 2 × 10 6 human HepG2 cells were inoculated onto a dorsal skin-fold chamber. One day after HepG2 inoculation, the experimental groups were fed oral daily with CUR or THC (300 mg/kg or 3000 mg/kg). On d 7, 14 and 21, the tumor microvasculature was observed using fluorescence videomicroscopy and capillary vascularity (CV) was measured. RESULTS:Pathological angiogenic features including microvascular dilatation, tortuosity, and hyper-permeability were observed. CUR and THC could attenuate these pathologic features. In HepG2-groups, the CV were significantly increased on d 7 (52.43%), 14 (69.17%), and 21 (74.08%), as compared to controls (33.04%,

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Roles of reactive oxygen species in angiopoietin‐1/tie‐2 receptor signaling

Cited by 116 publications

References 54 publications

NADPH Oxidase Activity Selectively Modulates Vascular Endothelial Growth Factor Signaling Pathways

NADPH Oxidase Activity Selectively Modulates Vascular Endothelial Growth Factor Signaling Pathways

N-benzyl-5-phenyl-1H-pyrazole-3-carboxamide promotes vascular endothelial cell angiogenesis and migration in the absence of serum and FGF-2

Anti-cancer and anti-angiogenic effects of curcumin and tetrahydrocurcumin on implanted hepatocellular carcinoma in nude mice

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