Wyniki wyszukiwania

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Opposite effect of prostaglandin-j2 on VEGF synthesis in normoxia and hypoxia

100%

Jozkowicz A., Nigisch A., Weigel G., Huk I., Dulak J.

Acta Biochimica Polonica

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2003

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tom 50

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nr Supplement 1

2

Role of NO in angiogenic activities of VEGF isoforms

86%

Jozkowicz A., Dulak J., Nigisch A., Partyka L., Weigel G., Huk I., Malinski T.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr Suppl.

3

Prostaglandin-J2 induces the endothelial synthesis of IL-8 independently of PPARgamma activation

86%

Jozkowicz A., Huk I., Nigisch A., Grzenkowicz J., Podhajska A., Weigel G., Dulak J.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr Suppl.

4

Nitric oxide mediates the mitogenic effects of insulin and vascular endothelial growth factor but not of leptin in endothelial cells

86%

Jozkowicz A., Pankiewicz J., Dulak J., Partyka L., Wybranska I., Huk I., Dembinska-Kiec A.

Acta Biochimica Polonica

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1999

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tom 46

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nr 3

The regulation of vascular wall homeostasis by nitric oxide (NO) generated by endothelium is being intensively studied. In the present paper, the involvement of NO in the vascular endothelial growth factor (VEGF), insulin or leptin-stimulated proliferation of human endothelial cells (HUVEC) was measured by [3H]thymidine or bromodeoxyuridine incorporation. VEGF and insulin, but not leptin, increased NO generation in HUVEC, as detected with ISO-NO electrode. Proliferation of HUVEC induced by leptin was not changed or was higher in the presence of L-Nω-nitro-L-arginine methyl ester (L-NAME) a nitric oxide synthase (NOS) inhibitor. In contrast, L-NAME blunted the proproliferative effect of VEGF and insulin. Furthermore, we demonstrated that, in human arterial smooth muscle cells (hASMC) transfected with endothelial NOS (eNOS) gene, the generation of biologically active VEGF protein was NO-dependent. Inhibition of NO generation by L-NAME decreased the synthesis of VEGF protein and attenuated HUVEC proliferation induced by conditioned media from transfected hASMC. Endothelium-derived NO seems to participate in VEGF and insulin, but not leptin, mitogenic activity. Additionally, the small amounts of NO released from endothelial cells, as mimicked by eNOS transfection into hASMC, may activate generation of VEGF in sub-endothelial smooth muscle cells, leading to increased synthesis of VEGF protein necessary for turnover and restitution of endothelial cells.

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In situ measurement of nitric oxide, superoxide and peroxynitrite during endotoxemia

86%

Brovkovych V., Patton S., Brovkovych S., Kiechle F., Huk I., Malinski T.

Journal of Physiology and Pharmacology

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1997

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tom 48

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nr 4

6

Prostaglandin-J2 upregulates expression of matrix metalloproteinase-1 independently of activation of peroxisome proliferator-activated receptor-gamma

86%

Jozkowicz A., Huk I., Nigisch A., Cisowski J., Weigel G., Dulak J.

Acta Biochimica Polonica

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2003

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tom 50

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nr 3

Peroxisome proliferator-activated receptor-y (PPARy) is a ligand-inducible nuclear receptor that functions as a transcription factor involved in lipid metabolism, inflammatory response and angiogenesis. The most potent endogenous PPARγ activator is 15-deoxy-Δ12,14,prostaglandin-J2 (15d-PGJ2), whereas synthetic ligands include the oral antidiabetic drugs thiazolidinediones (TZDs). Activation of PPARγ was reported to decrease the synthesis of matrix metalloproteinases (MMPs) in vascular smooth muscle cells and macrophages. We aimed to investigate the effect of PPARy ligands on expression of MMP-1 and urokinase plasminogen activator (uPA) in human microvascular endothelial cells (HMEC-1). We found that treatment of HMEC-1 with 15d-PGJ2 increased the synthesis of MMP-1 protein up to 168% comparing to untreated cells. TZDs (ciglitazone and troglitazone), more potent activators of PPAR in HMEC-1, did not influence MMP-1 production, arguing against the involvement of PPAR in this process. Importantly, the stimulatory effect of 15d-PGJ2 was reversed by the antioxidant N-acetyl-cysteine (NAC), suggesting a contribution of oxidative stress. We demonstrated also that 15d-PGJ2 did not change the activity of MMP-1 promoter, but increased the stability of MMP-1 mRNA. In contrast, 15d-PGJ2 very potently inhibited the synthesis of uPA. This effect was in part mimicked by ciglitazone and troglitazone implying an involvement of PPAR. Accordingly, NAC did not modify the inhibitory effect of 15d-PGJ2 on uPA expression. In conclusion, we postulate that 15d-PGJ2 may differently regulate the synthesis of proteases involved in angiogenesis: it upregulates MMP-1 expression in HMEC-1 through induction of oxidative stress, and inhibits uPA synthesis partly by activation of PPARγ.

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Lower levels of Caveolin-1 and higher levels of endothelial Nitric oxide synthase are observed in abdominal aortic aneurysm patients treated with simvastatin

72%

Kowalska K., Habrowska-Gorczynska D., Neumayer C., Bolliger M., Domenig C., Piastowska-Ciesielska A., Huk I., Piechota-Polanczyk A.

Acta Biochimica Polonica

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2018

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tom 65

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nr 1

Ograniczanie wyników

Opposite effect of prostaglandin-j2 on VEGF synthesis in normoxia and hypoxia

Role of NO in angiogenic activities of VEGF isoforms

Prostaglandin-J2 induces the endothelial synthesis of IL-8 independently of PPARgamma activation

Nitric oxide mediates the mitogenic effects of insulin and vascular endothelial growth factor but not of leptin in endothelial cells

In situ measurement of nitric oxide, superoxide and peroxynitrite during endotoxemia

Prostaglandin-J2 upregulates expression of matrix metalloproteinase-1 independently of activation of peroxisome proliferator-activated receptor-gamma

Lower levels of Caveolin-1 and higher levels of endothelial Nitric oxide synthase are observed in abdominal aortic aneurysm patients treated with simvastatin