Involvement of Beclin‑1 in axonal protection by short‑term hyperglycemia against TNF‑induced optic nerve damage.
Involvement of Beclin‑1 in axonal protection by short‑term hyperglycemia against TNF‑induced optic nerve damage.
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DOI：
10.3892/mmr.2018.9568
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发表时间：
2018-12
影响因子：
3.4
通讯作者：
Takagi H
中科院分区：
文献类型：
--
作者：
Sase K;Kitaoka Y;Tsukahara C;Takagi H
Beclin-1在自噬体形成中起关键作用。先前的研究表明，链脲佐菌素诱导的高血糖症（HG）减轻了肿瘤坏死因子（TNF）诱导的轴突丢失，上调了大鼠的自噬。本研究的目的是检查Beclin-1是否参与这种自噬机制。免疫印迹分析表明，HG上调Beclin-1蛋白的表达时，与normoprotein（NG）相比。玻璃体内注射TNF并不改变NG和HG视神经Beclin-1的表达。Beclin-1的免疫反应性被发现主要是在视神经的星形胶质细胞，然而，它也被观察到在HG组的神经丝。形态计量学分析显示，HG似乎有显着的改善效果轴突损失，这种改善效果被Beclin-1小干扰RNA部分阻止。这些结果表明Beclin-1可能存在于视神经的神经元和胶质细胞中，并且Beclin-1表达的增加可能至少部分地与HG的轴突保护有关。
Beclin-1 serves a pivotal role in autophagosome formation. A previous study demonstrated that streptozotocin-induced hyperglycemia (HG) ameliorates axonal loss induced by tumor necrosis factor (TNF) with upregulation of autophagy in rats. The aim of present study was to examine whether Beclin-1 is involved in this autophagy machinery. Immunoblot analysis of optic nerves demonstrated that HG upregulated Beclin-1 protein expression when compared with normoglycemia (NG). Intravitreal administration of TNF did not alter the optic nerve Beclin-1 expression in NG nor in HG. Beclin-1 immunoreactivity was revealed to be mainly in astrocytes in optic nerves; however, it was also observed in the neurofilaments of the HG group. Morphometric analysis revealed that HG appeared to have substantial ameliorative effects on axon loss and this ameliorative effect was partially prevented by Beclin-1 small interfering RNA. These results indicated that Beclin-1 may exist in neurons and glia in optic nerves and increased Beclin-1 expression may be at least partially associated with axonal protection by HG.
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