COMPLEMENT AND CLUSTERIN IN THE SPINAL-CORD DORSAL HORN AND GRACILE NUCLEUS FOLLOWING SCIATIC-NERVE INJURY IN THE ADULT-RAT
COMPLEMENT AND CLUSTERIN IN THE SPINAL-CORD DORSAL HORN AND GRACILE NUCLEUS FOLLOWING SCIATIC-NERVE INJURY IN THE ADULT-RAT
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DOI：
10.1016/0306-4522(95)00103-p
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发表时间：
1995-09-01
期刊：
影响因子：
3.3
通讯作者：
SVENSSON, M
中科院分区：
文献类型：
--
作者：
LIU, L;TORNQVIST, E;SVENSSON, M
我们提供的证据激活的补体级联反应在脊髓背角和薄束核在脑干坐骨神经横断在成年大鼠。免疫细胞化学分析表明，内源性免疫球蛋白G的免疫反应性，如F（ab '）（2）抗体免疫染色所示，以及补体因子C1，Clq，C3，C3d和C9在损伤的坐骨神经的适当的中央终止区。双标记免疫细胞化学的结果显示，一方面免疫球蛋白和补体因子与另一方面反应性小胶质细胞之间有很强的关联。然而，一些补体免疫反应性也被发现在神经胶质细胞，可能代表分泌的补体。用寡核苷酸探针原位杂交显示C3信使RNA显著增加，表明C3蛋白的局部合成。与补体激活平行，假定的补体抑制剂簇蛋白的免疫反应性增加，其与胶质细胞酸性蛋白阳性星形胶质细胞共定位。原位杂交结果显示，clusterin信使RNA的标记增加。这些结果表明，补体激活和上调补体抑制剂是突出的中枢反应，外周感觉神经损伤。因此，这些反应可能是初级感觉轴突和末梢中所谓的跨神经节退行性变化的重要因素。
We provide evidence for activation of the complement cascade in the dorsal horn of the spinal cord and in the gracile nucleus in the brainstem following sciatic nerve transection in the adult rat. Immunocytochemical analyses showed immunoreactivity for endogenous immunoglobulin G as shown by immunostaining with F(ab')(2) antibodies, as well as complement factors C1, Clq, C3, C3d and C9 in the appropriate central termination areas of the injured sciatic nerve. Results from double labelling immunocytochemistry showed a strong association between immunoglobulin and complement factors on the one hand and reactive microglia on the other. However, some complement immunoreactivity was also found in the neuropil, possibly representing secreted complement. In situ hybridization with an oligonucleotide probe showed a marked increase in C3 messenger RNA, indicating local synthesis of C3 protein. In parallel with activation of complement, there was an increased immunoreactivity for the putative complement inhibitor clusterin, which co-localized with glial fibrillary acidic protein-positive astrocytes. In situ hybridization showed an increased labelling of clusterin messenger RNA.These findings indicate that complement activation and up-regulation of complement inhibitors are prominent central responses to peripheral sensory nerve injury. These responses may therefore be important elements underlying so-called transganglionic degenerative changes in primary sensory axons and terminals.