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

被引:0
作者
M. H. Deininger
Michael Weller
Johannes Streffer
Michel Mittelbronn
Richard Meyermann
机构
[1] Institute of Brain Research,
[2] University of Tuebingen Medical School,undefined
[3] Calwer Str. 3,undefined
[4] D-72076 Tuebingen,undefined
[5] Germany e-mail: hirnforschung@uni-tuebingen.de Tel.: +49-7071-2982283,undefined
[6] Fax: +49-7071-294846,undefined
[7] Department of Neurology,undefined
[8] University of Tuebingen Medical School,undefined
[9] Tuebingen,undefined
[10] Germany,undefined
来源
Acta Neuropathologica | 1999年 / 98卷
关键词
Key words Glioma; Cyclooxygenase; Immunohistochemistry;
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摘要
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.
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页码:240 / 244
页数:4
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