Macrophage colony stimulating factor (M-CSF) exacerbates ALS disease in a mouse model through altered responses of microglia expressing mutant superoxide dismutase

被引：44

作者：

Gowing, Genevieve ^{[1
]}

Lalancette-Hebert, Melanie ^{[1
]}

Audet, Jean-Nicolas ^{[1
]}

Dequen, Florence ^{[1
]}

Julien, Jean-Pierre ^{[1
]}

机构：

[1] Univ Laval, Dept Psychiat & Neurosci, CHU Quebec, Ctr Rech, Quebec City, PQ G1V 4G2, Canada

来源：

EXPERIMENTAL NEUROLOGY | 2009年 / 220卷 / 02期

基金：

加拿大健康研究院;

关键词：

Motor neuron disease; Amyotraphic lateral sclerosis; Macrophage-colony stimulating factor (M-CSF); Microglia; Macrophage; Neuroinflammation; Superoxide dismutase 1 (SOD1); Transgenic mice; AMYOTROPHIC-LATERAL-SCLEROSIS; MOTOR-NEURON DEGENERATION; NECROSIS-FACTOR-ALPHA; PROMOTES FUNCTIONAL RECOVERY; INJURED SPINAL-CORD; WILD-TYPE MICROGLIA; EXTEND SURVIVAL; NITRIC-OXIDE; NEURODEGENERATIVE DISEASE; PROLIFERATING MICROGLIA;

D O I：

10.1016/j.expneurol.2009.08.021

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Macrophage colony stimulating factor (M-CSF) is a cytokine that regulates the Survival, proliferation and maturation of microglial cells. Administration of M-CSF can promote neuronal survival in various models of central nervous system (CNS) injury. Here, in an attempt to induce a neuroprotective microglial cell phenotype and enhance motor neuron survival, mutant SOD1(G37R) transgenic mice were treated, weekly, with M-CSF starting at onset of disease. Unexpectedly, M-CSF accelerated disease progression in SOD1(G37R) mouse model of ALS. The shortened survival of M-CSF-treated animals was associated with diminished muscle innervation and enhanced adoption of a macrophage-like phenotype by microglial cells characterised by the upregulation of pro-inflammatory cytokines TNF-alpha and IL-1 beta and of the phagocytic marker CD68. (C) 2009 Elsevier Inc. All rights reserved.

引用

页码：267 / 275

页数：9

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