补体C5调节慢性实验性变应性脑脊髓炎中胰岛素样生长因子结合蛋白的表达。
Complement C5 regulates the expression of insulin-like growth factor binding proteins in chronic experimental allergic encephalomyelitis.
作者信息
Cudrici Cornelia, Ito Takahiro, Zafranskaia Ekaterina, Weerth Susanna, Rus Violeta, Chen Hegang, Niculescu Florin, Soloviova Katerina, Tegla Cosmin, Gherman Adrian, Raine Cedric S, Shin Moon L, Rus Horea
机构信息
Department of Neurology, University of Maryland School of Medicine, Baltimore 21201, USA.
出版信息
J Neuroimmunol. 2008 Oct 15;203(1):94-103. doi: 10.1016/j.jneuroim.2008.06.040.
Abstract
Complement activation plays a central role in autoimmune demyelination. To explore the possible effects of C5 on post-inflammatory tissue repair, we investigated the transcriptional profile induced by C5 in chronic experimental allergic encephalomyelitis (EAE) using oligonucleotide arrays. We used C5-deficient (C5-d) and C5-sufficient (C5-s) mice to compare the gene expression profile and we found that 390 genes were differentially regulated in C5-s mice as compared to C5-d mice during chronic EAE. Among them, a group of genes belonging to the family of insulin-like growth factor binding proteins (IGFBP) and transforming growth factor (TGF)-beta3 were found most significantly differentially regulated by C5. The dysregulation of these genes suggests that these proteins might be responsible for the gliosis and lack of remyelination seen in C5-d mice with chronic EAE.
摘要
补体激活在自身免疫性脱髓鞘中起核心作用。为了探究C5对炎症后组织修复的可能影响，我们使用寡核苷酸阵列研究了慢性实验性变应性脑脊髓炎（EAE）中C5诱导的转录谱。我们使用C5缺陷（C5-d）和C5充足（C5-s）小鼠比较基因表达谱，发现在慢性EAE期间，与C5-d小鼠相比，C5-s小鼠中有390个基因受到差异调节。其中，一组属于胰岛素样生长因子结合蛋白（IGFBP）家族和转化生长因子（TGF）-β3的基因被发现受C5的差异调节最为显著。这些基因的失调表明，这些蛋白质可能是导致慢性EAE的C5-d小鼠出现胶质增生和髓鞘再生缺乏的原因。
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