gms | German Medical Science

57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

11. bis 14.05.2006, Essen

A1 adenosine receptor deficiency in the host brain promotes the growth of inoculated glioblastoma cells

Verlust des A1-Adenosin-Rezeptors im ZNS fördert das Wachstum induzierter Glioblastome

Meeting Abstract

  • corresponding author M. Synowitz - Department of Neurosurgery, Helios Hospital Berlin
  • R. Glass - Cellular Neuroscience Group, Max Delbrück Center for Molecular Medicine (MDC), Berlin
  • K. Faerber - Cellular Neuroscience Group, Max Delbrück Center for Molecular Medicine (MDC), Berlin
  • G. Kronenberg - Department of Psychiatry, Free University, Charité – CBF, Berlin
  • J. Schnermann - National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Health, Bethesda/USA
  • H. Kettenmann - Cellular Neuroscience Group, Max Delbrück Center for Molecular Medicine (MDC), Berlin

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie. Essen, 11.-14.05.2006. Düsseldorf, Köln: German Medical Science; 2006. DocP 05.62

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2006/06dgnc279.shtml

Veröffentlicht: 8. Mai 2006

© 2006 Synowitz 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 vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: In the present study, we have addressed the question whether deletion of A1 adenosine receptors affect glioblastoma – host interaction observed in A1AR deficient mice.

Methods: G261 glioblastoma cells stably expressing were inoculated into A1AR-/- mice and A1AR+/+ littermate controls. With this approach, we deleted the A1AR in the host cells, but not in the inoculated GL261 glioblastoma cells. Animals were sacrificed 14 days after GL261 inoculation and the tumor area was determined double-blinded in axial section at the maximal diameter. Immunofluorescent triple labeling was carried out on 40-µm-free-floating sections using a spectral confocal microscope.

Results: The tumor size in A1AR-/- mice was significantly larger as compared to A1AR+/+ mice (mean±SE, 0.96±0.09 mm for control (n=73); 1.69±0.03 mm for A1AR-/- mice (n=99)). There were no differences in neurological symptoms between the groups within the 14 days after GL261 inoculation. To analyze the cell populations from the host in the vicinity of the tumor cells, we studied the distribution of microglial cells and astrocytes in A1AR-/- and A1AR+/+ mice. Immunoreactivity for the macrophage / microglia marker Iba-1 revealed an accumulation of Iba-1 positive cells at the tumor border. In A1AR-/- mice the density and number of Iba-1 positive cells was significantly higher as compared to wild-type littermates. No differences in the GFAP-positive cell population was observed comparing A1AR-/- and A1AR+/+.

Conclusions: These results imply that A1AR modulate tumor growth and that microglial cells are the cellular candidates to mediate this effect.