G-CSF administration to adult mice stimulates the proliferation of microglia but does not modify the outcome of ischemic injury

被引:23
作者
Bartolini, Alice [1 ,2 ]
Vigliani, Maria-Claudia [4 ]
Magrassi, Lorenzo [5 ]
Vercelli, Alessandro [1 ,3 ]
Rossi, Ferdinando [1 ,2 ]
机构
[1] Cavalieri Ottolenghi Fdn NICO, Inst Neurosci, I-10043 Turin, Italy
[2] Univ Turin, Neurosci Inst Turin, Dept Neurosci, Physiol Sect, I-10125 Turin, Italy
[3] Univ Turin, Neurosci Inst Turin, Dept Anat Pharmacol & Forens Med, I-10125 Turin, Italy
[4] Univ Turin, Dept Neurosci, Div Neurol 2, I-10125 Turin, Italy
[5] Univ Pavia, Fdn IRCCS Policlin San Matteo, Dept Surg Sci, I-27100 Pavia, Italy
关键词
G-CSF; Medial cerebral artery occlusion; Hematopoietic cells; Brain repair; Cell proliferation; Bone marrow; HEMATOPOIETIC STEM-CELLS; BONE-MARROW; FOCAL ISCHEMIA; PURKINJE NEURONS; SUBACUTE PHASE; GROWTH-FACTORS; IN-VIVO; BRAIN; STROKE; RAT;
D O I
10.1016/j.nbd.2010.11.013
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Recent evidence suggests that adult bone marrow stem cells reduce tissue damage and promote repair following CNS ischemic injury. Since granulocyte-colony stimulating factor (G-CSF) mobilizes hematopoietic stem cells to the circulating compartment, here we tested whether administration of this drug modifies the outcome of a permanent occlusion of the middle cerebral artery in adult mice. To elucidate the behavior and fate of blood-borne cells in the ischemic brain, we produced chimeric animals, in which hematopoietic derivatives are genetically tagged. G-CSF administration enhances the proliferation of microglia in the uninjured CNS but has no effect on the amount of hematopoietic cells that infiltrate the ischemic tissue and on the size of the lesion. The blood-borne elements acquire different mesodermal identities but fail to adopt neural phenotypes, even though they occasionally fuse with Purkinje neurons. These results indicate that G-CSF treatment does not exert a significant beneficial effect on the ischemic injury. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:640 / 649
页数:10
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