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IGF binding protein alterations on periplaque oligodendrocytes in multiple sclerosis: Implications for remyelination.

机译:多发性硬化中斑块少突胶质细胞上的IGF结合蛋白改变:对髓鞘再生的影响。

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摘要

Why myelin repair greatly fails in multiple sclerosis (MS) is unclear. The insulin-like growth factor (IGF) system plays vital roles in oligodendrocyte development, survival, and myelin synthesis. We used immunohistochemistry to study IGF-I, IGF-I receptors and IGF binding proteins (IGFBPs) 1-6 on oligodendrocytes at the edges of chronic demyelinated plaques and normal appearing white matter of MS, and in cerebral white matter of controls without neurological disease. Oligodendrocytes in all conditions were immunoreactive for IGF-I, IGF-I receptors and IGFBPs-1-5. Oligodendrocytes at the edges of demyelinated plaques displayed enhanced immunoreactivity for IGF-I, IGF-I receptors, IGFBPs-1 and -6. Because increased expression of IGFBPs-1 and -6 has been associated with impaired synthesis of myelin proteins in oligodendrocyte lineage cells, pharmacological approaches to reduce their expression might be useful for promoting remyelination of axons in MS lesions.
机译:为何髓磷脂修复在多发性硬化症(MS)中大大失败的原因尚不清楚。胰岛素样生长因子(IGF)系统在少突胶质细胞的发育,存活和髓鞘合成中起着至关重要的作用。我们使用免疫组化方法研究了慢性脱髓鞘斑块边缘的少突胶质细胞和MS正常出现的白质以及无神经系统疾病的对照者的脑白质中IGF-I,IGF-I受体和IGF结合蛋白(IGFBPs)1-6 。在所有条件下,少突胶质细胞对IGF-1,IGF-1受体和IGFBPs-1-5具有免疫反应性。脱髓鞘斑块边缘的少突胶质细胞对IGF-1,IGF-1受体,IGFBP-1和-6的免疫反应增强。因为IGFBPs-1和-6的表达增加与少突胶质细胞系细胞中髓磷脂蛋白的合成受损有关,所以降低其表达的药理方法可能有助于促进MS病变轴突的髓鞘再生。

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