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首页> 外文期刊>The European Journal of Neuroscience >The transcriptional corepressor TPA-inducible sequence 7 regulates adult axon growth through cellular retinoic acid binding protein II expression.
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The transcriptional corepressor TPA-inducible sequence 7 regulates adult axon growth through cellular retinoic acid binding protein II expression.

机译：转录共抑制物TPA诱导序列7通过细胞视黄酸结合蛋白II表达调节成年轴突的生长。

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摘要

TPA-inducible sequence 7 (TIS7) expression is regulated in epithelial cells and acts as a transcriptional corepressor. Using a TIS7 knock-out mouse we demonstrated that TIS7 is involved in the process of muscle regeneration. In this study, we analysed the role of TIS7 in axon regeneration, applying primary neurone cultures derived from adult dorsal root ganglia (DRGs) of TIS7+/+ and TIS7-/- mice. TIS7-/- DRG neurones exhibited a significant decrease in axon initiation and maximal axon extension. In contrast, nerve growth factor-induced axon initiation and branching were significantly enhanced in cultures obtained from TIS7-/- DRGs when compared with wildtype ganglia, suggesting an inhibitory effect of TIS7 on nerve growth factor-stimulated axon growth. TIS7 overexpression in TIS7-/- DRG neurones caused their morphological appearance to revert back to the wildtype phenotype. Furthermore, the expression of cellular retinoic acid binding protein II (CRABP II), previously identified by us as a TIS7 target gene, was up-regulated in adult DRG sensory neurones from TIS7-/- mice. Overexpression of CRABP II in TIS7+/+ neurones strongly increased the number of branch points, making them morphologically similar to TIS7-/- neurones. Based on these results we propose that TIS7 inhibits CRABP II expression during axonal regeneration, thereby modulating retinoic acid signalling. Hence, neurite initiation and branching are regulated by a negative feedback mechanism involving TIS7 and CRABP II.
机译：TPA诱导序列7（TIS7）的表达在上皮细胞中受到调节，并起转录共抑制因子的作用。使用TIS7敲除小鼠，我们证明了TIS7参与肌肉再生过程。在这项研究中，我们分析了TIS7在轴突再生中的作用，应用了从TIS7 + / +和TIS7-/-小鼠的成年背根神经节（DRG）衍生的原代神经元培养物。 TIS7-/-DRG神经元在轴突起始和最大轴突扩展方面显示出明显的减少。相比之下，与野生型神经节相比，从TIS7-/-DRGs获得的培养物中神经生长因子诱导的轴突起始和分支显着增强，表明TIS7对神经生长因子刺激的轴突生长具有抑制作用。 TIS7-/-DRG神经元中的TIS7过表达导致其形态学外观恢复为野生型表型。此外，先前被我们确定为TIS7靶基因的细胞视黄酸结合蛋白II（CRABP II）的表达在TIS7-/-小鼠的成年DRG感觉神经元中被上调。在TIS7 + / +神经元中CRABP II的过表达极大地增加了分支点的数量，使其在形态上与TIS7-/-神经元相似。基于这些结果，我们提出TIS7在轴突再生过程中抑制CRABP II表达，从而调节视黄酸信号传导。因此，通过涉及TIS7和CRABP II的负反馈机制调节神经突的起始和分支。

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