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Microglia cyclooxygenase-2 activity in experimental gliomas: possible role in cerebral edema formation

Behnam Badie1, Jill M Schartner, Aaron R Hagar

  • 1Department of Neurological Surgery, University of Wisconsin School of Medicine, Madison, Wisconsin 53792, USA. badie@neurosurg.wisc.edu

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|February 11, 2003
PubMed
Abstract

Insights

Microglia in brain tumors produce prostaglandin E(2) (PGE(2)) via cyclooxygenase-2 (COX-2). Inhibiting COX-2 reduces brain edema, suggesting COX-2 inhibitors as potential treatments for malignant brain tumors.

Area of Science:

  • Neuroscience
  • Oncology
  • Inflammation Research

Background:

  • Malignant gliomas cause significant morbidity and mortality, often due to cerebral edema.
  • Inflammatory cells, particularly microglia, are implicated in brain edema formation.
  • Cyclooxygenase-2 (COX-2) is a key enzyme in arachidonic acid metabolism and inflammation.

Purpose of the Study:

  • To investigate the role of microglia-derived cyclooxygenase-2 (COX-2) in brain edema formation in a rodent glioma model.
  • To examine the expression and activity of COX-2 in microglia within the glioma microenvironment.

Main Methods:

  • Primary microglia cultures from rat C6 gliomas were analyzed for COX-2 expression using RT-PCR and Western blot.
  • Prostaglandin E(2) (PGE(2)) production was quantified via enzyme immunoassay.
  • Blood-tumor barrier permeability was assessed using magnetic resonance imaging in tumor-bearing rats treated with a COX-2 inhibitor (rofecoxib) or dexamethasone.

Main Results:

  • Microglia isolated from C6 gliomas exhibited high levels of PGE(2) production, dependent on COX-2 activity.
  • Treatment with rofecoxib significantly reduced blood-tumor barrier permeability, comparable to dexamethasone.
  • These findings indicate that microglia are a significant source of PGE(2) in gliomas, contributing to edema.

Conclusions:

  • Glioma-infiltrating microglia are a major source of PGE(2) through the COX-2 pathway.
  • COX-2 inhibitors show potential as therapeutic alternatives to glucocorticoids for managing peritumoral edema in malignant brain tumors.

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