Suppr超能文献

来自受损神经的逆向信号的性质,该信号在神经元中诱导白细胞介素-6信使核糖核酸。

Nature of the retrograde signal from injured nerves that induces interleukin-6 mRNA in neurons.

作者信息

Murphy P G, Borthwick L S, Johnston R S, Kuchel G, Richardson P M

机构信息

Division of Neurosurgery, Montreal General Hospital and McGill University, Montreal, Canada H3G 1A4.

出版信息

J Neurosci. 1999 May 15;19(10):3791-800. doi: 10.1523/JNEUROSCI.19-10-03791.1999.

Abstract

In previous studies, interleukin-6 was shown to be synthesized in approximately one-third of lumbar dorsal root ganglion neurons during the first week after nerve transection. In present studies, interleukin-6 mRNA was found to be induced also in axotomized facial motor neurons and sympathetic neurons. The nature of the signal that induces interleukin-6 mRNA in neurons after nerve injury was analyzed. Blocking of retrograde axonal transport by injection of colchicine into an otherwise normal nerve did not induce interleukin-6 mRNA in primary sensory neurons, but injection of colchicine into the nerve stump prevented induction of interleukin-6 mRNA by nerve transection. Therefore, it was concluded that interleukin-6 is induced by an injury factor arising from the nerve stump rather than by interruption of normal retrograde trophic support from target tissues or distal nerve segments. Next, injection into the nerve of a mast cell degranulating agent was shown to stimulate interleukin-6 mRNA in sensory neurons and systemic administration of mast cell stabilizing agents to mitigate the induction of interleukin-6 mRNA in sensory neurons after nerve injury. These data implicate mast cells as one possible source of the factors that lead to induction of interleukin-6 mRNA after nerve injury. In search of a possible function of inducible interelukin-6, neuronal death after nerve transection was assessed in mice with null deletion of the interleukin-6 gene. Retrograde death of neurons in the fifth lumbar dorsal root ganglion was 45% greater in knockout than in wild-type mice. Thus, endogenous interleukin-6 contributes to the survival of axotomized neurons.

摘要

在先前的研究中,神经横断后第一周,约三分之一的腰段背根神经节神经元可合成白细胞介素-6。在目前的研究中,发现轴突切断的面神经运动神经元和交感神经元中也可诱导白细胞介素-6信使核糖核酸。对神经损伤后诱导神经元中白细胞介素-6信使核糖核酸的信号性质进行了分析。向原本正常的神经中注射秋水仙碱阻断逆行轴突运输,并未在初级感觉神经元中诱导白细胞介素-6信使核糖核酸,但向神经残端注射秋水仙碱可防止神经横断诱导白细胞介素-6信使核糖核酸。因此,得出结论,白细胞介素-6是由神经残端产生的损伤因子诱导的,而非由靶组织或远端神经节段正常逆行营养支持的中断所诱导。接下来,向神经中注射肥大细胞脱颗粒剂可刺激感觉神经元中的白细胞介素-6信使核糖核酸,全身给予肥大细胞稳定剂可减轻神经损伤后感觉神经元中白细胞介素-6信使核糖核酸的诱导。这些数据表明肥大细胞是神经损伤后导致白细胞介素-6信使核糖核酸诱导的因素的一个可能来源。为了寻找诱导性白细胞介素-6的可能功能,在白细胞介素-6基因完全缺失的小鼠中评估了神经横断后的神经元死亡情况。与野生型小鼠相比,敲除小鼠第五腰段背根神经节中神经元的逆行死亡增加了45%。因此,内源性白细胞介素-6有助于轴突切断的神经元存活。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验