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A peripheral nerve reproduction control structure by one oxidized form galectin-1 instruction macrophage.

A peripheral nerve reproduction control structure by one oxidized form galectin-1 instruction macrophage.
一种由氧化型半乳糖凝集素-1指令巨噬细胞控制周围神经再生的结构。
批准号:
17500265
负责人:
HORIE Hidenori
金额:
$2.24万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2005
资助国家:
日本
项目状态:
已结题
起止时间:
2005 至 2006

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中文摘要
翻译
氧化半乳糖凝集素-1(GAL-1/0x)刺激巨噬细胞促进周围神经损伤后轴突再生。但是,GAL-1/0x的作用机制,即如何调控巨噬细胞,目前尚不清楚。本实验观察了Gal-/Ox对培养的大鼠腹腔巨噬细胞中白细胞介素1β(IL-1β)、白介素6(IL-6)、白血病抑制因子(LIF)和诱导型一氧化氮合酶(INOS)四种损伤相关分子表达的影响。RT-PCR分析显示,1 ng/mlGal-1/0x可上调IL-6和iNOS的mRNA表达,而Gal-1/0x对其余各组的表达无明显影响。升高的IL-6可能会促进周围神经的轴突再生,但上调iNOS,促进氧化,可能会损害再生神经。这个问题通过以下实验得到了解决。利用脂多糖刺激巨噬细胞促进细胞因子…的表达是一种典型的刺激物质更多的NE和iNOS。当10~100 ng/mlLPS作用于培养的巨噬细胞时,IL-1LIF、IL-6、β和iNOSmRNA的表达均上调。1 ng/mlGal-1/0x处理使其表达减少。Gal-1/0x浓度降至0.1 ng/ml时抑制作用减弱,0.01 ng/mlGal-1/0x处理后抑制作用不明显。这些结果表明,Gal-1/0x可能将IL-1LIF、IL-6、β和诱导型一氧化氮合酶的表达调节到合适的水平,否则可能会过度损伤损伤组织。已证实Galectin-1以还原形式存在于损伤周围神经的神经元、轴突和雪旺细胞中,氧化后分泌到细胞外间隙,转化为氧化型Galectin-1,Gal-1/0x可限制巨噬细胞适量分泌因子,从而促进修复。由于GAL-1/0x、巨噬细胞和内毒素在全身炎症中常见,GAL-1/0x有望改善炎症。较少
英文摘要
Oxidized galectin-1 (GAL-1/0x) stimulates macrophages to promote axonal regeneration in peripheral nerves after nerve injury. But, the mechanism of GAL-1/0x, how to regulate macrophages, remains to be clarified. Here we demonstrated effects of GAL-/Ox on mRNA expression of four injury related molecules, interleukin-1β (IL-1β), interleukin-6 (IL-6), leukemia inhibitory factor (LIF), and inducible NO synthase (iNOS) in cultured rat peritoneal macrophages. RT-PCR analysis revealed that IL-6 as well as iNOS mRNA expressions were up-regulated by the treatment with 1 ng/ml GAL-1/0x, but the other mRNA did not show significant differences by the application of GAL-1/0x. Increased IL-6 may promote axonal regeneration in peripheral nerves, but up-regulated iNOS, promoting oxidization, may damage regenerating nerves. This problem was resolved by the following experiments. Using lipopolysaccharide (LPS) is one of the typical substance to stimulate macrophages to promote mRNA expressions of cytoki … More nes and iNOS. When 10 to 100 ng/ml LPS was applied to cultured macrophages, mRNA expressions of IL-1β, IL-6, LIF, and iNOS were up-regulated. The treatment of 1 ng/ml GAL-1/0x reduced their expressions. This inhibition by GAL-1/0x treatment reduced with decreasing its concentration to 0.1 ng/ml and 0.01 ng/ml GAL-1/0x showed no significant inhibitory effect. These results indicate the possibility that GAL-1/0x regulates expressions of IL-1β, IL-6, LIF, and iNOS to a suitable level, otherwise damaging injured tissues in an excess. Since it has been proved that galectin-1 locates as a reduced form in neurons, their axons, and Schwann cells in injured peripheral nerves and is secreted into extra-cellular space to change into oxidized galectin-1 after oxidization, GAL-1/0x may restrict macrophages to secrete the factors in a proper amount resulting with the promotion of recovery. Since GAL-1/0x, macrophage, and LPS are commonly seen in general inflammation, GAL-1/0x is expected to improve inflammation. Less
期刊论文(36)
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会议论文
Regulation of the neuronal cell fate by ΔFosB and its downstream target, galectin-1.
ΔFosB 及其下游靶标 galectin-1 对神经元细胞命运的调节。
DOI: --
发表时间: 2005
期刊: Curr Drug Targets 6
影响因子: --
作者: [三五 一憲, 斎藤 春洋, 堀江 秀典, Kurushima H, Kadoya T, McGraw J, Horie H, Kadoya T, Horie H, Miura T]
通讯作者: Miura T
Editorial "Galectin-1 as an Essential Factor in Nervous System"
社论“Galectin-1 作为神经系统的重要因子”
DOI: --
发表时间: 2005
期刊: Curr Drug Targets 6
影响因子: --
作者: [Kurushima H, Y., Kadoya T, Horie H]
通讯作者: Horie H
Selective induction of delta-FosB in the brain after transient forebrain ischemia accompanied by an increased expression of galectin-1, and
短暂前脑缺血后大脑中选择性诱导 delta-FosB,并伴有 galectin-1 表达增加,以及
DOI: --
发表时间: 2005
期刊: Cell Death Differ 12
影响因子: --
作者: [Kurushima H, 他3名, Horie H, 他5名, Nakabeppu Y.]
通讯作者: Nakabeppu Y.
Regulation of galecin-1 expression by axotomy in rat primary afferent neurons.
通过轴索切断术调节大鼠初级传入神经元中的 Galecin-1 表达。
DOI: --
发表时间: 2005
期刊: Exp Neurol. 195
影响因子: --
作者: [三五 一憲, 斎藤 春洋, 堀江 秀典, Kurushima H, Kadoya T, McGraw J]
通讯作者: McGraw J
共 30 条
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