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Hypoxia inducible factor-1 is involved in growth factor, glucocorticoid and hypoxia mediated regulation of vascular endothelial growth factor-A in human meningiomas

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons80600

Wu,  Yonghe
Dept. Clinical Research, Max Planck Institute of Psychiatry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons110919

Lucia,  Kristin
Dept. Clinical Research, Max Planck Institute of Psychiatry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons80539

Stalla,  Günter Karl
Dept. Clinical Research, Max Planck Institute of Psychiatry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons80491

Renner,  Ulrich
Dept. Clinical Research, Max Planck Institute of Psychiatry, Max Planck Society;

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Zitation

Wu, Y., Lucia, K., Lange, M., Kuhlen, D., Stalla, G. K., & Renner, U. (2014). Hypoxia inducible factor-1 is involved in growth factor, glucocorticoid and hypoxia mediated regulation of vascular endothelial growth factor-A in human meningiomas. JOURNAL OF NEURO-ONCOLOGY, 119(2), 263-273. doi:10.1007/s11060-014-1503-5.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0024-60FA-6
Zusammenfassung
In meningiomas, neovascularization through angiogenesis is essential for tumor expansion. As the vascular endothelial growth factor-A (VEGF-A) plays an outstanding role in this process, we have studied basal VEGF-A release and some aspects of its regulation in 46 meningiomas and in Ben-Men-1 cells in vitro. Among two putative VEGF-A stimulating growth factors tested, TGF-1 beta was more potent than TGF-alpha in enhancing VEGF-A secretion. Hypoxia-mimicking conditions induced by CoCl2 treatment also strongly increased VEGF-A secretion. The synthetic glucocorticoid dexamethasone (DEX) potently suppressed both basal and growth factor or CoCl2-induced VEGF-A release. All these effects were also seen in the Ben-Men-1 cell line in which studies on the role of HIF-1 in the regulation of VEGF-A showed that not only hypoxia but also the growth factors induced HIF-1 alpha and DEX suppressed HIF-1 alpha induction. Therefore, in Ben-Men-1 cells with HIF-1 alpha knock-down the effects of hypoxia, growth factors and DEX on VEGF-A production were strongly impaired. This clearly indicates that HIF-1 not only regulates hypoxia-induced VEGF-A production but also mediates at least in part the effects of growth factors and DEX on VEGF-A synthesis and release. Our findings show the complexity of VEGF-A regulation in meningiomas and point to new options for the pharmacological treatment of these tumors.