Erythropoietin dampens injury-induced microglial motility

被引：14

作者：

Mitkovski, Miso ^{[1
]}

Dahm, Liane ^{[2
]}

Heinrich, Ralf ^{[3
]}

Monnheimer, Mathieu ^{[2
]}

Gerhart, Simone ^{[2
]}

Stegmueller, Judith ^{[4
,5
]}

Hanisch, Uwe-Karsten ^{[6
]}

Nave, Klaus-Armin ^{[5
,7
]}

Ehrenreich, Hannelore ^{[2
,5
]}

机构：

[1] Max Planck Inst Expt Med, Light Microscopy Facil, D-37075 Gottingen, Germany

[2] Max Planck Inst Expt Med, Clin Neurosci, D-37075 Gottingen, Germany

[3] Univ Gottingen, Inst Zool, Dept Cellular Neurobiol, D-37073 Gottingen, Germany

[4] Max Planck Inst Expt Med, Cellular & Mol Neurobiol Grp, D-37075 Gottingen, Germany

[5] Ctr Nanoscale Microscopy & Mol Physiol Brain CNMP, Gottingen, Germany

[6] Univ Gottingen, Inst Neuropathol, D-37073 Gottingen, Germany

[7] Max Planck Inst Expt Med, Dept Neurogenet, D-37075 Gottingen, Germany

来源：

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM | 2015年 / 35卷 / 08期

关键词：

ATP; brain injury; migration; process protrusion; Rac1; IN-VIVO; BRAIN; ACTIVATION; GTPASES; ATP; RHO; NEURODEGENERATION; LESION; CELLS; RAC1;

D O I：

10.1038/jcbfm.2015.100

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Traumatic brain injury causes progressive brain atrophy and cognitive decline. Surprisingly, an early treatment with erythropoietin (EPO) prevents these consequences of secondary neurodegeneration, but the mechanisms have remained obscure. Here we show by advanced imaging and innovative analytical tools that recombinant human EPO, a clinically established and neuroprotective growth factor, dampens microglial activity, as visualized also in vivo by a strongly attenuated injury-induced cellular motility.

引用

页码：1233 / 1236

页数：4

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