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Spatiotemporal expression of neurogenic locus notch homolog protein 1 in developing caudal spinal cord of fetuses with anorectal malformations from ETU-fed rats.
Journal of Molecular Histology ( IF 2.9 ) Pub Date : 2020-08-11 , DOI: 10.1007/s10735-020-09900-w
Zhonghua Yang 1 , Huimin Jia 1 , Yuzuo Bai 1 , Weilin Wang 1
Affiliation  

Complications, such as fecal soiling, incontinence, and constipation, are major health issues for patients with anorectal malformations (ARMs) after surgery. Dysplasia of the caudal spinal cord is an increasingly pivotal area in the field of postoperative complications for patients with ARMs. However, the existing research has not fully defined the mechanism underlying ARMs development. The neurogenic locus notch homolog (Notch) signaling pathway comprises several highly conserved proteins that are involved in spinal cord developmental processes. In the present study, the emerging role of Notch1 in fetal lumbosacral spinal cords was investigated in a rat model of ARMs using ethylene thiourea. Immunohistochemical staining, western blot and quantitative reverse transcription real-time polymerase chain reaction were utilized to analyze spatiotemporal expression of Notch1 on embryonic days (E) 16, E17, E19, and E21. The expression levels of the neuronal marker neurofilament and recombination signal-binding protein-J protein were evaluated for temporal correlations to Notch1 expression. The results implied that Notch1 expression was reduced in lumbosacral spinal cord neurons of ARMs embryos compared to control embryos. These results showed that, in ARMs embryos decreased Notch1 expression is related to the dysplasia of the caudal spinal cord during embryogenesis, indicating that Notch signaling may participate pathogenic embryonic lumbosacral spinal development and may be associated with postoperative complications of ARMs.



中文翻译:

在由ETU喂养的大鼠的肛门直肠畸形胎儿的发育中的尾椎脊髓中,神经源性刻痕缺口同源蛋白1的时空表达。

诸如粪便弄脏,大小便失禁和便秘等并发症是肛门直肠畸形(ARMs)术后患者的主要健康问题。在ARM患者的术后并发症领域中,尾椎发育不良是一个日益重要的领域。但是,现有研究尚未完全定义ARM开发的基础机制。神经源性刻痕缺口同源物(Notch)信号传导途径包含与脊髓发育过程有关的几种高度保守的蛋白质。在本研究中,在使用乙烯硫脲的ARM大鼠模型中研究了Notch1在胎儿腰s脊髓中的新兴作用。免疫组织化学染色 免疫印迹和定量逆转录实时聚合酶链反应用于分析Notch1在胚胎第(E)16,E17,E19和E21天的时空表达。评估神经元标记神经丝和重组信号结合蛋白-J蛋白的表达水平与Notch1表达的时间相关性。结果表明,与对照胚胎相比,Notch1表达在ARM胚胎的腰spin脊髓神经元中降低。这些结果表明,在ARMs胚胎中,Notch1表达的降低与胚胎发生过程中尾脊髓的异常增生有关,这表明Notch信号可能参与了病原性胚胎腰s脊柱的发育,并且可能与ARMs的术后并发症有关。E17,E19和E21 评估神经元标记神经丝和重组信号结合蛋白-J蛋白的表达水平与Notch1表达的时间相关性。结果暗示,与对照胚胎相比,Notch1表达在ARM胚胎的腰s脊髓神经元中减少。这些结果表明,在ARMs胚胎中,Notch1表达的降低与胚胎发生过程中尾脊髓的异常增生有关,这表明Notch信号可能参与了病原性胚胎腰s脊柱的发育,并且可能与ARMs的术后并发症有关。E17,E19和E21 评价神经元标记神经丝和重组信号结合蛋白-J蛋白的表达水平与Notch1表达的时间相关性。结果暗示,与对照胚胎相比,Notch1表达在ARM胚胎的腰s脊髓神经元中减少。这些结果表明,在ARMs胚胎中,Notch1表达的降低与胚胎发生过程中尾脊髓的异常增生有关,这表明Notch信号可能参与了病原性胚胎腰s脊柱的发育,并且可能与ARMs的术后并发症有关。结果暗示,与对照胚胎相比,Notch1表达在ARM胚胎的腰s脊髓神经元中减少。这些结果表明,在ARMs胚胎中,Notch1表达的降低与胚胎发生过程中尾脊髓的异常增生有关,这表明Notch信号可能参与了病原性胚胎腰s脊柱的发育,并且可能与ARMs的术后并发症有关。结果表明,与对照胚胎相比,Notch1表达在ARM胚胎的腰s脊髓神经元中降低。这些结果表明,在ARMs胚胎中,Notch1表达的降低与胚胎发生过程中尾脊髓的异常增生有关,这表明Notch信号可能参与了病原性胚胎腰s脊柱的发育,并且可能与ARMs的术后并发症有关。

更新日期:2020-08-12
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