The conditioning lesion effect on sympathetic neurite outgrowth is dependent on gp130 cytokines.
The conditioning lesion effect on sympathetic neurite outgrowth is dependent on gp130 cytokines.
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DOI：
10.1016/j.expneurol.2010.01.019
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发表时间：
2010-06
影响因子：
5.3
通讯作者：
Zigmond, R. E.
中科院分区：
文献类型：
--
作者：
Sachs, H. Hyatt;Rohrer, H.;Zigmond, R. E.
关键词：
交感神经元，就像感觉神经元一样，在条件性损伤后增加轴突生长。对白血病抑制因子(LIF)基因敲除动物的研究表明，感觉神经元的条件性损伤效应部分依赖于这种细胞因子；然而，对交感神经元的类似研究表明没有这种作用。与从缺乏相关细胞因子IL-6(IL-6)的小鼠身上提取的感觉神经元进行的可比性研究得出了相互矛盾的结果。Lif和IL-6属于被称为gp130家族的细胞因子家族，因为它们作用于包含亚单位gp130的受体。在交感神经节中，切断轴突导致其中四种细胞因子(LIF、IL-6、IL-11和成本蛋白M)的mRNA增加。为了测试这个细胞因子家族作为一个整体在交感神经元条件性损伤反应中的作用，对去甲肾上腺素能神经元中gp130选择性消除的小鼠进行了研究。切断SCG的节后轴突，7天后取出神经节，在外植体和分离细胞培养中观察轴突生长情况。在这两个系统中，野生型动物的神经元在条件性损伤后显示出增强的生长。相比之下，突变动物的神经元没有增强。尽管突变小鼠中激活转录因子3(ATF3)的表达增加，但这种对突起生长的刺激作用仍然存在。这些研究表明，条件性损伤后促进交感神经元生长的刺激依赖于gp130细胞因子信号，并在没有这些细胞因子信号的情况下被阻断，尽管ATF3增加。
Sympathetic neurons, like sensory neurons, increase neurite outgrowth after a conditioning lesion. Studies in leukemia inhibitory factor (LIF) knockout animals showed that the conditioning lesion effect in sensory neurons is dependent in part on this cytokine; however, similar studies on sympathetic neurons revealed no such effect. Comparable studies with sensory neurons taken from mice lacking the related cytokine interleukin-6 (IL-6) have yielded conflicting results. LIF and IL-6 belong to a family of cytokines known as the gp130 family because they act on receptors containing the subunit gp130. In sympathetic ganglia, axotomy leads to increases in mRNA for four of these cytokines (LIF, IL-6, IL-11, and on-costatin M). To test the role of this family of cytokines as a whole in the conditioning lesion response in sympathetic neurons, mice in which gp130 was selectively eliminated in noradrenergic neurons were studied. The postganglionic axons of the SCG were transected, and seven days later the ganglia were removed and neurite outgrowth was measured in explant and dissociated cell cultures. In both systems, neurons from wild type animals showed enhanced growth after a conditioning lesion. In contrast, no enhancement occurred in neurons from mutant animals. This lack of stimulation of outgrowth occurred despite an increase in expression of activating transcription factor 3 (ATF3) in the mutant mice. These studies demonstrate that stimulation of enhanced growth of sympathetic neurons after a conditioning lesion is dependent on gp130 cytokine signaling and is blocked in the absence of signaling by these cytokines in spite of an increase in ATF3.
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影响因子：
4.7
作者：
Dowsing, BJ;Morrison, WA;Kilpatrick, TJ
通讯作者：
Kilpatrick, TJ
DOI：
10.1073/pnas.91.15.7109
发表时间：
1994-07-19
影响因子：
11.1
作者：
BANNER, LR;PATTERSON, PH
通讯作者：
PATTERSON, PH
DOI：
10.1023/a:1006988528655
发表时间：
1998-06-01
期刊：
JOURNAL OF NEUROCYTOLOGY
影响因子：
--
作者：
Hou, XE;Lundmark, K;Dahlström, AB
通讯作者：
Dahlström, AB
影响因子：
3
作者：
Habecker, Beth A.;Sachs, Hilary Hyatt;Rohrer, Hermann;Zigmond, Richard E.
通讯作者：
Zigmond, Richard E.
影响因子：
4.7
作者：
Gardiner, NJ;Cafferty, WBJ;Thompson, SWN
通讯作者：
Thompson, SWN