gms | German Medical Science

62. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Polnischen Gesellschaft für Neurochirurgen (PNCH)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

07. - 11. Mai 2011, Hamburg

Mesenchymal stem-like cells in malignant gliomas represent a hypoxia-resistant subpopulation

Meeting Abstract

  • F. Faber - Department of Neurosurgery, Ludwig-Maximilians- University, Klinikum Großhadern, Munich, Germany
  • G. Ke-Tai - Department of Neurosurgery, Ludwig-Maximilians- University, Klinikum Großhadern, Munich, Germany
  • J. Thorsteinsdottir - Department of Neurosurgery, Ludwig-Maximilians- University, Klinikum Großhadern, Munich, Germany
  • D. Jaeger - Department of Neurosurgery, Ludwig-Maximilians- University, Klinikum Großhadern, Munich, Germany
  • V. Albrecht - Department of Neurosurgery, Ludwig-Maximilians- University, Klinikum Großhadern, Munich, Germany
  • C. Schichor - Department of Neurosurgery, Ludwig-Maximilians- University, Klinikum Großhadern, Munich, Germany

Deutsche Gesellschaft für Neurochirurgie. Polnische Gesellschaft für Neurochirurgen. 62. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Polnischen Gesellschaft für Neurochirurgen (PNCH). Hamburg, 07.-11.05.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. DocMO.07.06

DOI: 10.3205/11dgnc043, URN: urn:nbn:de:0183-11dgnc0435

Veröffentlicht: 28. April 2011

© 2011 Faber et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

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Objective: Enhanced proliferation, metabolic stress, necrosis and hypoxia are hallmarks of malignant gliomas. Emerging data suggest that malignant gliomas consist of diverse cell identities that produce a broad variety of factors in order to escape cell death through the loss of oxygenation, such as hypoxia-inducible factors (HIF1, HIF2) and erythropoietin (EPO) / erythropoietin receptor (EPO-R). In this study we isolated mesenchymal progenitor cells out of human glioblastoma specimen and compared the expression profile of hypoxia-related factors as well as the migration and proliferation capacity under normoxic and hypoxic conditions with malignant glioma cells.

Methods: The expression of HIF1, HIF2, EPO, EPO-R and VEGF were investigated in mesenchymal progenitor cells isolated from glioblastoma, as well as in glioma cell lines under normoxic and hypoxic conditions by RT-PCR. Furthermore, we characterized their hypoxia-induced migratory and proliferation behavior using the spheroid-based migration assay on laminin and proliferation assays.

Results: The expression of HIF2, EPO, EPO-R and VEGF increased under hypoxic conditions in glioma cell lines and mesenchymal progenitor cells. HIF1 was detected heterogeneously without a significant upregulation under hypoxia. Hypoxic conditions showed a pro-migratory effect on glioma cells lines, which is reduced in mesenchymal progenitor cells. In addition, the hypoxia-induced upregulation of hypoxia-related factors was only conducive to the proliferation of mesenchymal progenitor cells. In contrast the glioma cell lines showed decreased proliferation under hypoxia.

Conclusions: Expression of the hypoxia-related factors EPO, EPO-R and VEGF is not only limited to glioma cell lines but is mainly upregulated in glioma-isolated mesenchymal progenitor cells. Furthermore, our results suggest that different cells identities within a brain tumor show different responses to hypoxia in their proliferation and migration capacity.