一种新的甲状腺激素介导的HSV-1基因表达和复制调控是特异性的神经元细胞,并与染色质凝聚的破坏有关。

Feng Chen, Jay Palem, Matthew Balish, Robert Figliozzi, Amakoe Ajavon, S Victor Hsia
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引用次数: 6

摘要

先前我们在神经母细胞瘤细胞系神经2a细胞(N2a)中发现,甲状腺激素(T3)通过组蛋白修饰和染色质重塑,通过其核受体TR调控单纯疱疹病毒1型(HSV-1)基因的表达和复制。这一观察结果表明,T3的调节可能是神经元特异性的,并与HSV-1的潜伏期和再激活有关。在这项研究中,我们的体外潜伏期/再激活模型表明,去除T3可以抑制HSV-1的复制并有利于再激活。转染研究和感染实验表明,TR/T3在神经元细胞中抑制HSV-1胸苷激酶(TK),而在非神经元细胞中不抑制TK。进一步的研究表明,RCC1(染色体凝聚1调节因子)被隔离,但在病毒感染N2a细胞时有效检测到。Western blot分析表明,T3的加入抑制了感染后RCC1的表达。在TR/T3的影响下,神经细胞感染后RCC1的减少可能导致病毒复制/基因表达受到抑制,从而促进潜伏期。总之,这些结果表明,TR/T3介导的调节是神经元细胞特异性的,差异染色体凝聚可能在这一过程中起关键作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

A Novel Thyroid Hormone Mediated Regulation of HSV-1 Gene Expression and Replication is Specific to Neuronal Cells and Associated with Disruption of Chromatin Condensation.

A Novel Thyroid Hormone Mediated Regulation of HSV-1 Gene Expression and Replication is Specific to Neuronal Cells and Associated with Disruption of Chromatin Condensation.

A Novel Thyroid Hormone Mediated Regulation of HSV-1 Gene Expression and Replication is Specific to Neuronal Cells and Associated with Disruption of Chromatin Condensation.

A Novel Thyroid Hormone Mediated Regulation of HSV-1 Gene Expression and Replication is Specific to Neuronal Cells and Associated with Disruption of Chromatin Condensation.

Previously we showed that thyroid hormone (T3) regulated the Herpes Simplex Virus Type -1 (HSV-1) gene expression and replication through its nuclear receptor TR via histone modification and chromatin remodeling in a neuroblastoma cell line neuro-2a cells (N2a). This observation suggested that T3 regulation may be neuron-specific and have implication in HSV-1 latency and reactivation. In this study, our in vitro latency/reactivation model demonstrated that removal of T3 can de-repress the HSV-1 replication and favor reactivation. Transfection studies and infection assays indicated that HSV-1 thymidine kinase (TK), a key viral gene during reactivation, was repressed by TR/T3 in cells with neuronal origin but not in non-neuronal cells. Additional studies showed that RCC1 (Regulator of Chromosome Condensation 1) was sequestered but efficiently detected upon viral infection in N2a cells. Western blot analyses indicated that addition of T3 repressed the RCC1 expression upon infection. It is likely that diminution of RCC1 upon infection in neuronal cells under the influence of TR/T3 may lead to repression of viral replication/gene expression thus promote latency. Together these results demonstrated that TR/T3 mediated regulation is specific to neuronal cells and differential chromosome condensation may play a critical role in this process.

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