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The NADPH Oxidase Nox4 mediates tumour angiogenesis.

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Title: The NADPH Oxidase Nox4 mediates tumour angiogenesis.
Authors: Helfinger, V., Henke, N., Harenkamp, S., Walter, M., Epah, J., Penski, C., Mittelbronn, M., Schröder, K.
Source: Acta Physiologica. Apr2016, Vol. 216 Issue 4, p435-446. 12p. 3 Color Photographs, 1 Black and White Photograph, 1 Chart, 2 Graphs.
Subjects: NADPH oxidase, Neovascularization, Tumors, Carcinogens research, Fibrosarcoma
Abstract: Aim The aim of this work was to identify the role of the NADPH oxidase Nox4 for tumour angiogenesis in a slow-growing tumour model in mice. Methods Tumour angiogenesis was studied in tumours induced by the carcinogen 3-methylcholanthrene ( MCA) in wild-type and Nox knockout mice. Mice were killed when the tumour reached a diameter of 1.5 cm and tumour tissue was used for histological and molecular analysis. Results 3-methylcholanthrene induced fibrosarcoma in wild-type, Nox1y/-, Nox2y/- and Nox4-/- mice. Histological analysis of vessel density using anti- CD31 staining showed a significant 38% reduction in tumour vascularization in fibrosarcomas of Nox4-/- mice. In contrast, tumour angiogenesis was doubled in Nox1 knockout mice, whereas knockout of Nox2 had no effect on tumour-vessel density. As underlying mechanisms, we identified a defect in hypoxia signalling in Nox4-/- mice. Hypoxia-inducible factor 1-alpha (Hif-1 α) accumulation in the tumours was attenuated as was the expression of the Hif-1 α-dependent pro-angiogenic genes vascular endothelial growth factor -A, glucose transporter 1 and adrenomedullin. Conclusion By regulating the tumour-vessel density through stabilization of Hif-1 α and induction of VEGF expression, Nox4 promotes tumour angiogenesis and may represent a novel target for anti-angiogenic tumour therapy. [ABSTRACT FROM AUTHOR]
Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: The NADPH Oxidase Nox4 mediates tumour angiogenesis.
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  Data: <searchLink fieldCode="AR" term="%22Helfinger%2C+V%2E%22">Helfinger, V.</searchLink><br /><searchLink fieldCode="AR" term="%22Henke%2C+N%2E%22">Henke, N.</searchLink><br /><searchLink fieldCode="AR" term="%22Harenkamp%2C+S%2E%22">Harenkamp, S.</searchLink><br /><searchLink fieldCode="AR" term="%22Walter%2C+M%2E%22">Walter, M.</searchLink><br /><searchLink fieldCode="AR" term="%22Epah%2C+J%2E%22">Epah, J.</searchLink><br /><searchLink fieldCode="AR" term="%22Penski%2C+C%2E%22">Penski, C.</searchLink><br /><searchLink fieldCode="AR" term="%22Mittelbronn%2C+M%2E%22">Mittelbronn, M.</searchLink><br /><searchLink fieldCode="AR" term="%22Schröder%2C+K%2E%22">Schröder, K.</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Acta+Physiologica%22">Acta Physiologica</searchLink>. Apr2016, Vol. 216 Issue 4, p435-446. 12p. 3 Color Photographs, 1 Black and White Photograph, 1 Chart, 2 Graphs.
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  Data: <searchLink fieldCode="DE" term="%22NADPH+oxidase%22">NADPH oxidase</searchLink><br /><searchLink fieldCode="DE" term="%22Neovascularization%22">Neovascularization</searchLink><br /><searchLink fieldCode="DE" term="%22Tumors%22">Tumors</searchLink><br /><searchLink fieldCode="DE" term="%22Carcinogens+research%22">Carcinogens research</searchLink><br /><searchLink fieldCode="DE" term="%22Fibrosarcoma%22">Fibrosarcoma</searchLink>
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  Label: Abstract
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  Data: Aim The aim of this work was to identify the role of the NADPH oxidase Nox4 for tumour angiogenesis in a slow-growing tumour model in mice. Methods Tumour angiogenesis was studied in tumours induced by the carcinogen 3-methylcholanthrene ( MCA) in wild-type and Nox knockout mice. Mice were killed when the tumour reached a diameter of 1.5 cm and tumour tissue was used for histological and molecular analysis. Results 3-methylcholanthrene induced fibrosarcoma in wild-type, Nox1y/-, Nox2y/- and Nox4-/- mice. Histological analysis of vessel density using anti- CD31 staining showed a significant 38% reduction in tumour vascularization in fibrosarcomas of Nox4-/- mice. In contrast, tumour angiogenesis was doubled in Nox1 knockout mice, whereas knockout of Nox2 had no effect on tumour-vessel density. As underlying mechanisms, we identified a defect in hypoxia signalling in Nox4-/- mice. Hypoxia-inducible factor 1-alpha (Hif-1 α) accumulation in the tumours was attenuated as was the expression of the Hif-1 α-dependent pro-angiogenic genes vascular endothelial growth factor -A, glucose transporter 1 and adrenomedullin. Conclusion By regulating the tumour-vessel density through stabilization of Hif-1 α and induction of VEGF expression, Nox4 promotes tumour angiogenesis and may represent a novel target for anti-angiogenic tumour therapy. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1111/apha.12625
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              Text: Apr2016
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