TrkA immunoreactivity in reactive astrocytes in human neurodegenerative diseases and colchicine-treated rats
TrkA immunoreactivity in reactive astrocytes in human neurodegenerative diseases and colchicine-treated rats
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DOI：
10.1007/s004010050924
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发表时间：
1998-11-01
影响因子：
12.7
通讯作者：
Ferrer, I
中科院分区：
文献类型：
--
作者：
Aguado, F;Ballabriga, J;Ferrer, I
研究表明，神经生长因子（NGF）的使用能够抑制几种神经退行性疾病的组织损伤。作为了解NGF在神经退行性过程中星形胶质反应中可能的功能作用的第一步，我们分析了NGE TrkA功能受体在伴有反应性星形细胞增生的人类神经退行性疾病以及人类星形细胞瘤中的表达。我们将这些结果与秋水仙碱诱导的成年大鼠细胞损伤后反应性星形胶质细胞的观察结果进行了比较。在人脑中，在许多不相关的疾病中，包括阿尔茨海默病、亨廷顿病、进行性核上性麻痹、多发性硬化症、克雅氏病、多灶性脑白质病和残余缺氧脑病，在反应性星形胶质细胞中观察到强TrkA免疫反应性。II级和III级星形细胞瘤的肿瘤星形细胞表现出较强的TrkA免疫反应性。在大鼠脑中，机械针损伤和秋水仙碱处理后的反应性星形胶质细胞表现出强烈的TrkA免疫反应性。TrkA受体存在于不同人类神经退行性疾病的反应性星形胶质细胞和实验诱导的大鼠模型，以及肿瘤星形胶质细胞中，这表明NGF可能参与了星形胶质细胞对不同类型损伤和肿瘤增殖的反应。由于星形胶质细胞能够产生NGF，这种神经营养因子可能在表达trka的反应性和肿瘤性胶质细胞中作为自分泌或旁分泌因子发挥作用。
It has been shown that nerve growth factor (NGF) administration is capable of curbing tissue damage in several neurodegenerative disorders. As a first step to learning about the possible functional role of NGF in the astroglial response during neurodegeneration, we have analyzed the expression of the functional receptor for NGE TrkA, in human neurodegenerative diseases which are accompanied by reactive astrocytosis, as well as in human astrocytomas. We have compared these results with those observed in reactive astrocytes following colchicine-induced cellular damage to adult rats. In the human brain, strong TrkA immunoreactivity is observed in reactive astrocytes in a number of unrelated diseases, including Alzheimer's disease, Huntington's disease, progressive supranuclear palsy, multiple sclerosis, Creutzfeldt-Jakob disease, multifocal leukoencephalopathy and residual hypoxic encephalopathy. Neoplastic astrocytes in grade II and III astrocytomas display strong TrkA immunoreactivity. In the rat brain, reactive astrocytes following mechanical needle injury and colchicine administration show strong TrkA immunoreactivity. The presence of TrkA receptors in reactive astrocytes from different human neurodegenerative diseases and experimentally induced models in rats, and in neoplastic astrocytes suggests that NGF may participate in the astroglial response to different types of injury and neoplastic proliferation. Since astroglial cells are capable of producing NGF, it is plausible that this neurotrophin may function as an autocrine or paracrine factor in TrkA-expressing reactive and neoplastic glial cells.