Nerve injury stimulates the secretion of apolipoprotein E by nonneuronal cells.
Nerve injury stimulates the secretion of apolipoprotein E by nonneuronal cells.
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DOI：
10.1073/pnas.83.4.1130
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发表时间：
1986-02
影响因子：
11.1
通讯作者：
G. Snipes;C. McGuire;J. Norden;J. Freeman
中科院分区：
文献类型：
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作者：
G. Snipes;C. McGuire;J. Norden;J. Freeman
神经创伤引起非神经元细胞分泌的蛋白质组成的显著变化。这些蛋白质中最突出的是37 kDa蛋白质，其表达与神经发育、变性和再生的时间过程相关。我们现在报告，37 kDa的蛋白质是载脂蛋白E（apoE）。我们生产了一种特异性的抗血清对37 kDa的蛋白质分离从以前粉碎的神经。该抗血清识别大鼠血清中的一种36 kDa蛋白，我们已将其纯化并鉴定为apoE。抗37-kDa抗血清还识别高密度和极低密度脂蛋白真实样品电泳转移印迹上的apoE。神经37-kDa蛋白与载脂蛋白E通过双向电泳共迁移，共享相似的氨基酸组成，并与抗血清对真正的载脂蛋白E反应。纯化的apoE特异性阻断非神经元细胞合成的[35 S]甲硫氨酸标记的37-kDa蛋白的免疫沉淀。因此，根据其分子量、等电点、氨基酸组成和免疫学性质，我们得出结论，37-kDa蛋白质是apoE。我们还采用光镜免疫组织化学定位载脂蛋白E神经损伤。在视神经病变的大鼠中，37-kDa抗血清特异性结合到退化的视神经束和外侧膝状体核和上级丘的视网膜受体层。我们认为，apoE是由吞噬细胞在神经损伤后合成的，其目的是动员轴突变性后产生的脂质。
Nerve trauma initiates significant changes in the composition of proteins secreted by nonneuronal cells. The most prominent of these proteins is a 37-kDa protein, whose expression correlates with the time course of nerve development, degeneration, and regeneration. We now report that the 37-kDa protein is apolipoprotein E (apoE). We produced a specific antiserum against the 37-kDa protein isolated from previously crushed nerves. This antiserum recognizes a 36-kDa protein in rat serum that we have purified and identified as apoE. The anti-37-kDa antiserum also recognizes apoE on electrophoretic transfer blots of authentic samples of high and very low density lipoproteins. The nerve 37-kDa protein comigrates with apoE by two-dimensional electrophoresis, shares a similar amino acid composition, and reacts with an antiserum against authentic apoE. The purified apoE specifically blocks the immunoprecipitation of [35S]methionine-labeled 37-kDa protein synthesized by nonneuronal cells. Thus, on the basis of its molecular mass, isoelectric point, amino acid composition, and immunological properties, we conclude that the 37-kDa protein is apoE. We also used light microscopic immunohistochemistry to localize apoE following nerve injury. In rats with optic nerve lesions, the 37-kDa antiserum bound specifically to the degenerating optic tracts and to the retino-recipient layers of the lateral geniculate nucleus and the superior colliculus. We propose that apoE is synthesized by phagocytic cells in response to nerve injury for the purpose of mobilizing lipids produced as a consequence of axon degeneration.