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.
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
中文摘要
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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
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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
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:
[McGraw J, 他3名, Horie H, 他2名, Ramer MS., Horie H.]
通讯作者:
Horie H.
共 30 条
BASIC RESEARCH FOR EFFECT OF OXIDISED GALECTIN-1 ON PERIODONTAL DISEASE THROUGH MACROPHAGE
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批准号:20592438
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.0万
-
财政年份:2008
-
负责人:HORIE Hidenori
-
依托单位:
Novel Factor Oxidized Galectin-1 Advances Functional Recovery after Peripheral Nerve Injury
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批准号:12680758
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.37万
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财政年份:2000
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负责人:HORIE Hidenori
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依托单位:
Enhancement of neural regeneration and neural survival in peripheral nervous system by Novel Liver Derived Neuronal Activator
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批准号:07680849
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.6万
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财政年份:1995
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负责人:HORIE Hidenori
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依托单位:
Mechanism of new regeneration activating factor of aged nervous tissue secreted from hepatocytes and its determination with vitro immunization
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批准号:04836020
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.22万
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财政年份:1992
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负责人:HORIE Hidenori
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依托单位:
Study of changes of neuronal membrane functions with aging by tissue culture method
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批准号:63570041
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.28万
-
财政年份:1988
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负责人:HORIE Hidenori
-
依托单位:
国内基金
海外基金
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批准年份:2023
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TIPE2调控巨噬细胞M2极化改善睑板腺功能障碍的作用机制研究
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批准年份:2023
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Macrophage和Treg在移植免疫调节中的相互作用及其机制研究
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