gms | German Medical Science

55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

25. bis 28.04.2004, Köln

Adenosine A1 receptors act as a key man in glial tumours

Bedeutung von Adenosin-A1-Rezeptoren für das biologische Verhalten glialer Hirntumore

Meeting Abstract

  • corresponding author Michael Synowitz - Klinik für Neurochirurgie, HELIOS Klinikum Berlin, Klinikum Buch, Berlin; AG Zelluläre Neurowissenschaften, MDC Berlin-Buch, Berlin
  • M. Glaß - AG Zelluläre Neurowissenschaften, MDC Berlin-Buch, Berlin
  • D. Markovic - AG Zelluläre Neurowissenschaften, MDC Berlin-Buch, Berlin
  • H. Kettenmann - AG Zelluläre Neurowissenschaften, MDC Berlin-Buch, Berlin
  • J. Kiwit - Klinik für Neurochirurgie, HELIOS Klinikum Berlin, Klinikum Buch, Berlin

Deutsche Gesellschaft für Neurochirurgie. Ungarische Gesellschaft für Neurochirurgie. 55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie. Köln, 25.-28.04.2004. Düsseldorf, Köln: German Medical Science; 2004. DocMO.04.08

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2004/04dgnc0051.shtml

Veröffentlicht: 23. April 2004

© 2004 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 vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective

Adenosine is an ubiquitous nucleoside present in all body cells. It is released from metabolically active or stressed cells and subsequently acts as a regulatory molecule through binding to specific adenosine cell surface receptors. In this study we have addressed the question whether extracellular adenosine modulates growth of glial tumour cells and proposed that adenosine A1 receptors might mediate proliferative effects.

Methods

Expression of adenosine A1 receptor (AA1R) were examined by Western blot analysis, immunocytochemistry, and immunofluorescent double staining in rat and mice glial tumour cells, primary cultures of rat and mice neuroglia and human tumour material. Organotypical brain slice cultures were prepared from 16-day-old C57BL/6-mices and Fisher rats. Coronal slices of 250µm thickness were cut and placed in wells filled with standard culture medium. F98 rat glioma cells and mice G261 glioma cells were co-transfected with enhanced green fluorescent protein (pegfp-N1) using LipofectAmin. Thousand cells were solved in 0.1µl and injected into the basal ganglia of each slice via stereotactic device. Specific AA1R agonists and antagonist were added daily. Single tumour cell invasion and proliferation was observed by confocal laser scanning microscopy from day 1 to 7 and analysed using software ImagePro.

Results

Neuroglia and glial tumour express the AA1R receptor in all tested species. Interestingly microglia is the major source of AA1R expression and exhibit significantly in the tumour border. Activation of the AA1R receptor using the specific agonist CPA inhibit invasion as well as proliferation over time and off day three compared to the control group. Inhibition of the AA1R receptor using the specific antagonist CGS15943 showed a significant increase on tumour invasion and migration.

Conclusions

Our results support the idea that extracellular adenosine inhibits cell proliferation in glial tumour cells. The effect seems to conduct via cAMP-coupled adenosine A1 receptors. Further experiments have to reveal the role of AA1R on microglia and the importance for microglia - tumour interaction.