Acta Neuropathologica

, Volume 98, Issue 3, pp 240–244

Patterns of cyclooxygenase-1 and -2 expression in human gliomas in vivo

  • M. H. Deininger
  • Michael Weller
  • Johannes Streffer
  • Michel Mittelbronn
  • Richard Meyermann
Regular paper

DOI: 10.1007/s004010051075

Cite this article as:
Deininger, M., Weller, M., Streffer, J. et al. Acta Neuropathol (1999) 98: 240. doi:10.1007/s004010051075

Abstract

Cyclooxygenases (COX, prostaglandin endoperoxide synthases, PGG/H synthases) are potent mediators of inflammation. While COX-1 is constitutively expressed in a wide range of tissues, COX-2 is cytokine inducible. Although COX-1 expression is observed in normal tissue, enhanced COX-2 expression has been attributed a key role in the development of edema, impeding blood flow and immunomodulation observed in pathologically altered tissues. Here, we have analyzed the expression of COX-1 and COX-2 in 50 gliomas and 10 control brains with no neuropathological alterations by immunohistochemistry; 22 glioblastoma multiforme, 9 anaplastic astrocytomas, 5 protoplasmic astrocytomas, 1 gemistocytic astrocytoma and 13 fibrillary astrocytomas were included in the study. Compared with control brains, accumulation of COX-1 was detected in 20–50% of all cells in both low- and high-grade gliomas. Double-labeling experiments revealed COX-1 expression in subsets of macrophages/ microglial cells within the tumor parenchyma and in areas of infiltrative tumor growth. Of the COX-1-positive cells, 90% expressed MHC class II antigens. No COX-1 immunoreactivity was observed in tumor cells. COX-2-positive cells accumulated in tumor cells and in single macrophages/microglial cells in the immediate vicinity of necroses. Further studies are required to determine whether COX-2 is involved in the development of necrosis or, more likely, whether COX-2 is a part of the tumor tissue response to necrosis.

Key words GliomaCyclooxygenaseImmunohistochemistry

Copyright information

© Springer-Verlag Berlin Heidelberg 1999

Authors and Affiliations

  • M. H. Deininger
    • 1
  • Michael Weller
    • 2
  • Johannes Streffer
    • 2
  • Michel Mittelbronn
    • 1
  • Richard Meyermann
    • 1
  1. 1.Institute of Brain Research, University of Tuebingen Medical School, Calwer Str. 3, D-72076 Tuebingen, Germany e-mail: hirnforschung@uni-tuebingen.de Tel.: +49-7071-2982283, Fax: +49-7071-294846DE
  2. 2.Department of Neurology, University of Tuebingen Medical School, Tuebingen, GermanyDE