Patterns of cyclooxygenase-1 and-2 expression in human gliomas in vivo
Patterns of cyclooxygenase-1 and-2 expression in human gliomas in vivo
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DOI：
10.1007/s004010051075
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发表时间：
1999-09-01
影响因子：
12.7
通讯作者：
Meyermann, R
中科院分区：
文献类型：
--
作者：
Deininger, MH;Weller, M;Meyermann, R
环氧合酶(COX、前列腺素内源性过氧化物合成酶、PGG/H合成酶)是炎症反应的重要介质。虽然COX-1在广泛的组织中有结构性表达，但COX-2是细胞因子诱导的。虽然COX-1在正常组织中有表达，但在病理改变的组织中观察到的COX-2表达增强被认为是导致水肿、阻碍血流和免疫调节的关键因素。本研究采用免疫组织化学方法检测了50例脑胶质瘤和10例正常脑组织中COX-1和COX-2的表达，包括22例多形性胶质母细胞瘤、9例间变性星形细胞瘤、5例原浆型星形细胞瘤、1例生殖细胞性星形细胞瘤和13例纤维性星形细胞瘤。与对照组相比，在低级别和高级别胶质瘤中，COX-1在所有细胞中都有20%-50%的积聚。双标记实验显示，COX-1在肿瘤实质内的巨噬细胞/小胶质细胞亚群和肿瘤浸润性生长区域表达。在COX-1阳性细胞中，90%表达MHC-II类抗原。肿瘤细胞中未见COX-1免疫反应。COX-2阳性细胞聚集在肿瘤细胞和单个巨噬细胞/小胶质细胞中。需要进一步的研究来确定COX-2是否参与了坏死的发展，或者更有可能的是，COX-2是否是肿瘤组织对坏死的反应的一部分。
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.