Experimental diffuse axonal injury induces enhanced neuronal C5a receptor mRNA expression in rats
Experimental diffuse axonal injury induces enhanced neuronal C5a receptor mRNA expression in rats
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DOI：
10.1016/s0169-328x(97)00189-7
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发表时间：
1997-10-15
期刊：
影响因子：
--
通讯作者：
Barnum, SR
中科院分区：
文献类型：
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作者：
Stahel, PF;Kossmann, T;Barnum, SR
一些研究表明补体系统参与创伤性脑损伤（TBI）的病理生理学。由于鞘内产生的过敏毒素C5a已被证明介导中枢神经系统内的炎症反应，我们试图通过原位杂交来表征实验性弥漫性轴索损伤（DAI）大鼠脑中C5a受体（C5aR，CD88）mRNA的细胞表达。DAI诱导后4h，脑膜和侧脑室中可见表达C5aR mRNA的浸润性白细胞。浸润的C5aR阳性细胞的数量逐渐增加，创伤后24小时。在脑实质内，C5aR mRNA表达上调首先见于小脑浦肯野细胞在8小时内。在24小时后TBI，C5aR mRNA的表达是广泛的双边整个皮质和小脑，细胞表达被限制在锥体神经元和浦肯野细胞。C5aR转录信号在神经元上的强度在创伤后96小时进一步增加。C5 a与神经元上受体的配体结合可能介导以前未知的功能，从而可能导致TBI后的神经毒性和继发性神经元损伤。(C)1997年Elsevier Science B.V.
Several studies suggest the involvement of the complement system in the pathophysiology of traumatic brain injury (TBI). Since the intrathecal generation of anaphylatoxin C5a has been shown to mediate inflammatory effects within the central nervous system, we sought to characterize the cellular expression of the mRNA for the C5a receptor (C5aR, CD88) in brains of rats with experimental diffuse axonal injury (DAI) by in situ hybridization. Infiltrating leukocytes expressing C5aR mRNA were seen in meninges and lateral ventricles as early as 4 h after induction of DAI. The number of infiltrating C5aR-positive cells increased gradually up to 24 h after trauma. Within the brain parenchyma, up-regulation of C5aR mRNA expression was first seen in cerebellar Purkinje cells within 8 h. At 24 h after TBI, expression of C5aR mRNA was widespread bilaterally throughout the cortex and cerebellum, the cellular expression being restricted to pyramidal neurons and Purkinje cells. The intensity of C5aR transcript signals on neurons increased further up to 96 h after trauma. Ligand binding of C5a to its receptor on neurons might mediate previously unknown functions, thus possibly leading to neurotoxicity and secondary neuronal damage after TBI. (C) 1997 Elsevier Science B.V.