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三碘甲状腺原氨酸受体在神经鞘瘤和神经纤维瘤中的差异表达:施万细胞 - 轴突相互作用的作用

Differential expression of triiodothyronine receptors in schwannoma and neurofibroma: role of Schwann cell-axon interaction.

作者信息

Walter I B, Deruaz J P, de Tribolet N

机构信息

Institute of Histology and Embryology, Lausanne, Switzerland.

出版信息

Acta Neuropathol. 1995;90(2):142-9. doi: 10.1007/BF00294313.

Abstract

Regulation of gene expression in Schwann cells may be determined, at least in part, by the interaction of these cells with axons. Two peripheral nerve tumors, neurofibroma and schwannoma, represent good tools for studying Schwann cell activity in the presence or absence of axon action. In the present work we studied the expression of triiodothyronine receptors (T3R) by Schwann cells in these two tumors and also in adult normal sciatic nerve. Confirming the results of the histological examination, immunostaining of the neurofilaments showed the presence of fascicles or scattered axons in all neurofibroma sections studied. In these neurofibromas, Schwann cells did not express T3R immunoreactivity. Furthermore, in adult normal sciatic nerve, Schwann cells which ensheathed axons were devoid of any T3R expression. In contrast, in schwannoma, the complete absence of axons was demonstrated by the lack of neurofilament immunostaining. Here, Schwann cells deprived of axonal interaction displayed clear T3R immunoreactivity. In schwannoma cell cultures, Schwann cells continued to express T3R, even in cultures treated with medium that had been conditioned with rat sensory neurons. On the basis of these results, we suggest that, beside the possible regulatory mechanisms for T3R, the synthesis of T3R is regulated, at least in part, by Schwann cell-axon interaction.

摘要

雪旺氏细胞中基因表达的调控可能至少部分地由这些细胞与轴突的相互作用所决定。两种周围神经肿瘤,神经纤维瘤和神经鞘瘤,是研究有或没有轴突作用时雪旺氏细胞活性的良好工具。在本研究中,我们研究了这两种肿瘤以及成年正常坐骨神经中雪旺氏细胞三碘甲状腺原氨酸受体(T3R)的表达。神经丝免疫染色证实了组织学检查的结果,显示在所研究的所有神经纤维瘤切片中均存在束状或散在的轴突。在这些神经纤维瘤中,雪旺氏细胞不表达T3R免疫反应性。此外,在成年正常坐骨神经中,包裹轴突的雪旺氏细胞没有任何T3R表达。相反,在神经鞘瘤中,神经丝免疫染色的缺乏证明完全没有轴突。在这里,缺乏轴突相互作用的雪旺氏细胞显示出明显的T3R免疫反应性。在神经鞘瘤细胞培养物中,雪旺氏细胞继续表达T3R,即使在用大鼠感觉神经元条件培养基处理的培养物中也是如此。基于这些结果,我们认为,除了T3R可能的调控机制外,T3R的合成至少部分地受雪旺氏细胞 - 轴突相互作用的调控。

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