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在自身免疫性青光眼模型中,单独的S100与联合HSP 27时对视网膜神经节细胞具有相同的破坏作用。

S100 alone has the same destructive effect on retinal ganglion cells as in combination with HSP 27 in an autoimmune glaucoma model.

作者信息

Casola Christina, Schiwek Jennifer E, Reinehr Sabrina, Kuehn Sandra, Grus Franz H, Kramer Martin, Dick H Burkhard, Joachim Stephanie C

机构信息

Experimental Eye Research Institute, Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892, Bochum, Germany.

出版信息

J Mol Neurosci. 2015 May;56(1):228-36. doi: 10.1007/s12031-014-0485-2. Epub 2015 Jan 11.

DOI:10.1007/s12031-014-0485-2
PMID:25577368
Abstract

As previously shown, immunization with ocular antigens, like heat shock protein 27 (HSP 27), leads to retinal ganglion cell loss in an autoimmune glaucoma model. Aim of this study was to assess how immunization with S100 alone and in combination with HSP 27 affects retinal ganglion and macroglia cells. Rats were immunized with S100 or S100 plus HSP 27 (COMB). Neuronal cell density was evaluated on Nissl-stained flatmounts. Immunized groups showed a significant neuronal cell loss (S100, p = 0.005; COMB, p = 0.0005). A significant loss of retinal ganglion cells was also observed in both immunized groups on Brn-3a stained retinal cross-sections (S100, p = 0.003; COMB, p = 0.001). An increase in GFAP(+) area was noted in both groups (S100, p = 0.01; COMB, p = 0.001). In contrary, vimentin staining was not altered (S100/COMB, p > 0.05). In summary, immunization with solely S100 leads to retinal ganglion cell damage and reactive gliosis. While the combination of S100 plus HSP 27 also caused retinal ganglion cell loss and a glia response, the combination of the two antigens did not cause additional damage or more severe cell loss. We assume that both antigens might interact, possibly having inhibitory effects on each other and thus preventing additional damage to the retina.

摘要

如先前所示,在自身免疫性青光眼模型中,用眼部抗原(如热休克蛋白27,HSP 27)进行免疫会导致视网膜神经节细胞丢失。本研究的目的是评估单独用S100以及S100与HSP 27联合免疫如何影响视网膜神经节细胞和大胶质细胞。用S100或S100加HSP 27(联合组)对大鼠进行免疫。在尼氏染色的平铺标本上评估神经元细胞密度。免疫组显示出显著的神经元细胞丢失(S100组,p = 0.005;联合组,p = 0.0005)。在Brn - 3a染色的视网膜横切面上,两个免疫组也均观察到视网膜神经节细胞的显著丢失(S100组,p = 0.003;联合组,p = 0.001)。两组中均观察到GFAP(+)面积增加(S100组,p = 0.01;联合组,p = 0.001)。相反,波形蛋白染色未改变(S100/联合组,p > 0.05)。总之,单独用S100免疫会导致视网膜神经节细胞损伤和反应性胶质增生。虽然S100加HSP 27的联合免疫也导致视网膜神经节细胞丢失和胶质细胞反应,但两种抗原联合并未造成额外损伤或更严重的细胞丢失。我们推测这两种抗原可能相互作用,可能对彼此具有抑制作用,从而防止对视网膜造成额外损伤。

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本文引用的文献

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J Mol Neurosci. 2014 Feb;52(2):216-24. doi: 10.1007/s12031-013-0125-2. Epub 2013 Oct 3.
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Inflammatory demyelination induces glia alterations and ganglion cell loss in the retina of an experimental autoimmune encephalomyelitis model.炎症性脱髓鞘导致实验性自身免疫性脑脊髓炎模型中视网膜的神经胶质细胞改变和神经节细胞丢失。
J Neuroinflammation. 2013 Oct 4;10:120. doi: 10.1186/1742-2094-10-120.
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Retinal ganglion cell loss is accompanied by antibody depositions and increased levels of microglia after immunization with retinal antigens.
Mol Biol Rep. 2022 Jun;49(6):5107-5115. doi: 10.1007/s11033-022-07222-6. Epub 2022 Feb 25.
4
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J Neuroinflammation. 2020 Dec 14;17(1):375. doi: 10.1186/s12974-020-02012-y.
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Synapse and Receptor Alterations in Two Different S100B-Induced Glaucoma-Like Models.两种不同 S100B 诱导的青光眼样模型中的突触和受体改变。
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