Involvement of astrocytes in purine-mediated reparative processes in the brain
Involvement of astrocytes in purine-mediated reparative processes in the brain
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DOI：
10.1016/s0736-5748(00)00084-8
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发表时间：
2001-07-01
影响因子：
1.8
通讯作者：
Di Iorio, P
中科院分区：
文献类型：
--
作者：
Ciccarelli, R;Ballerini, P;Di Iorio, P
星形胶质细胞在生理条件下参与多种布兰功能，参与神经元发育、突触活动和细胞外环境的稳态控制。它们还积极参与脑损伤引发的过程，旨在限制和修复布兰损伤。嘌呤在中枢神经系统（CNS）的许多急性和慢性疾病的病理生理学中起重要作用。星形胶质细胞是脑内嘌呤的主要来源。它们释放基于腺嘌呤的嘌呤，例如腺苷和三磷酸腺苷。或基于鸟嘌呤的嘌呤，例如鸟苷和三磷酸鸟苷。在生理条件下，在病理条件下释放更多的嘌呤。星形胶质细胞表达几种腺嘌呤嘌呤受体亚型P1和P2。基于鸟嘌呤的嘌呤的受体正在被表征。特异性胞外酶如核苷酸酶、腺苷脱氨酶和可能的嘌呤核苷磷酸化酶，在从星形胶质细胞释放后代谢腺嘌呤和鸟嘌呤基嘌呤。这通过减少核苷酸和核苷与特定膜结合位点的相互作用来调节核苷酸和核苷的作用。基于腺嘌呤的核苷酸通过P2介导的细胞内[Ca 2 +]和异戊二烯化蛋白的增加刺激星形胶质细胞增殖。腺苷也可通过A（2）受体刺激星形胶质细胞增殖，但主要通过A（1）和/或A（3）受体抑制星形胶质细胞增殖，从而控制由P2受体触发的过度反应性星形胶质细胞增生。A（2）受体的激活还刺激星形胶质细胞产生营养因子，如神经生长因子、S100 β蛋白和转化生长因子β，其有助于保护神经元免受损伤。鸟苷刺激星形胶质细胞输出腺嘌呤基嘌呤，此外，它直接触发这些细胞增殖并产生大量的神经保护因子。这些数据表明，腺嘌呤和鸟嘌呤为基础的嘌呤释放大量的损伤或死亡的细胞的中枢神经系统可能作为：信号启动脑修复机制广泛涉及星形胶质细胞。(C)2001 ISDN。由Elsevier Science Ltd.出版，版权所有。
Astrocytes are involved in multiple blain functions in physiological conditions, participating in neuronal development, synaptic activity and homeostatic control of the extracellular environment. They also actively participate in the processes triggered by brain injuries, aimed at limiting and repairing blain damages. Purines may play a significant role in the pathophysiology of numerous acute and chronic disorders of the central nervous system (CNS). Astrocytes are the main source of cerebral purines. They release either adenine-based purines, e.g. adenosine and adenosine triphosphate. or guanine-based purines, e.g. guanosine and guanosine triphosphate. in physiological conditions and release even more of these purines in pathological conditions. Astrocytes express several receptor subtypes of P1 and P2 types for adenine-based purines. Receptors for guanine-based purines are being characterised. Specific ecto-enzymes such as nucleotidases, adenosine deaminase and, likely, purine nucleoside phosphorylase, metabolise both adenine- and guanine-based purines after release from astrocytes. This regulates the effects of nucleotides and nucleosides by reducing their interaction with specific membrane binding sites. Adenine-based nucleotides stimulate astrocyte proliferation by a P2-mediated increase in intracellular [Ca2+] and isoprenylated proteins. Adenosine also, via A(2) receptors, may stimulate astrocyte proliferation, but mostly, via A(1) and/or A(3) receptors, inhibits astrocyte proliferation, thus controlling the excessive reactive astrogliosis triggered by P2 receptors. The activation of A(2) receptors also stimulates astrocytes to produce trophic factors, such as nerve growth factor, S100 beta protein and transforming growth factor beta, which contribute to protect neurons against injuries. Guanosine stimulates the output of adenine-based purines from astrocytes and in addition it directly triggers these cells to proliferate and to produce large amount of neuroprotective factors. These data indicate that adenine- and guanine-based purines released in large amounts from injured or dying cells of CNS may act as: signals to initiate brain repair mechanisms widely involving astrocytes. (C) 2001 ISDN. Published by Elsevier Science Ltd. All rights reserved.