胸腺肽β4通过与G-肌动蛋白结合促进肌动蛋白聚合,从而促进斑马鱼毛氏轴突再生。

IF 4.4 1区 生物学 Q1 BIOLOGY BMC Biology Pub Date : 2024-10-23 DOI:10.1186/s12915-024-02045-2
Zheng Song, Along Han, Bing Hu
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引用次数: 0

摘要

背景:胸腺肽β4(Tβ4)是一种单体肌动蛋白结合蛋白,在生物活动中发挥着多种作用。然而,关于 Tβ4 在中枢轴突再生中的作用的一些研究却得出了相互矛盾的结果。以往的研究主要集中在培养细胞上,导致缺乏体内实验证据。因此,我们利用斑马鱼幼体毛氏细胞单轴突损伤模型来研究Tβ4在体内中枢轴突再生中的作用:结果:我们的研究结果表明,敲除Tβ4会阻碍轴突再生,而过表达Tβ4会促进轴突再生。而且,这种促进作用是通过 Tβ4 和 G-actin 之间的相互作用介导的。此外,我们的研究结果表明,Tβ4与G-肌动蛋白的结合促进了肌动蛋白的聚合而非解聚。在快速逃逸行为测试中,轴突受损的幼虫对尾部肌肉的控制能力受损,导致尾部无法正常弯曲,这被称为直尾现象。直尾比例与轴突再生长度呈显著负相关,这表明它是评估快速逃逸行为恢复情况的一个新指标。最后,研究结果表明,过表达 Tβ4 能有效恢复毛特纳细胞介导的快速逃逸行为的功能:我们的研究结果提供了 Tβ4 通过与 G-actin 结合促进体内中枢轴突再生的证据,并表明 Tβ4 可作为一种潜在的多肽药物用于临床治疗。
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Thymosin β4 promotes zebrafish Mauthner axon regeneration by facilitating actin polymerization through binding to G-actin.

Background: Thymosin beta 4 (Tβ4) is a monomeric actin-binding protein that plays many roles in biological activities. However, some studies on the role of Tβ4 in central axon regeneration have yielded contradictory results. Previous research has focused primarily on cultured cells, leading to a deficiency in in vivo experimental evidence. Therefore, we used a single axon injury model of Mauthner cells in zebrafish larvae to investigate the role of Tβ4 in central axon regeneration in vivo.

Results: Our results demonstrated that knockout of Tβ4 impaired axon regeneration, whereas overexpression of Tβ4 promoted axon regeneration. Moreover, this promotion is mediated through the interaction between Tβ4 and G-actin. Furthermore, our results suggest that the binding of Tβ4 to G-actin promotes actin polymerization rather than depolymerization. In the rapid escape behavior test, larvae with damaged axons presented impaired tail muscle control, resulting in a lack of normal tail bending, termed the straight tail phenomenon. The proportion of straight tails was significantly negatively correlated with axon regeneration length, suggesting that it is a new indicator for assessing rapid escape behavior recovery. Finally, the results showed that the overexpression of Tβ4 effectively restored the functionality of rapid escape behaviors mediated by Mauthner cells.

Conclusions: Our results provide evidence that Tβ4 promotes central axon regeneration in vivo through binding to G-actin and suggest that Tβ4 could serve as a potential polypeptide drug for clinical therapy.

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来源期刊
BMC Biology
BMC Biology 生物-生物学
CiteScore
7.80
自引率
1.90%
发文量
260
审稿时长
3 months
期刊介绍: BMC Biology is a broad scope journal covering all areas of biology. Our content includes research articles, new methods and tools. BMC Biology also publishes reviews, Q&A, and commentaries.
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