Granulocyte-Macrophage Colony-Stimulating Factor Enhances Leptomeningeal Collateral Growth Induced by Common Carotid Artery Occlusion

Granulocyte-Macrophage Colony-Stimulating Factor Enhances Leptomeningeal Collateral Growth Induced by Common Carotid Artery Occlusion
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DOI:
10.1161/strokeaha.107.503433
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发表时间:
2008-06
期刊:
影响因子:
8.3
通讯作者:
K. Todo;K. Kitagawa;Tsutomu Sasaki;E. Omura-Matsuoka;Y. Terasaki;N. Oyama;Y. Yagita;M. Hori
K. Todo;K. Kitagawa;Tsutomu Sasaki;E. Omura-Matsuoka;Y. Terasaki;N. Oyama;Y. Yagita;M. Hori
中科院分区:
医学1区
文献类型:
--
作者:
K. Todo;K. Kitagawa;Tsutomu Sasaki;E. Omura-Matsuoka;Y. Terasaki;N. Oyama;Y. Yagita;M. Hori

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背景和目的-粒细胞-巨噬细胞集落刺激因子(GM-CSF)已被报道可加速大鼠脑Willis环的侧支生长(动脉生成)。然而,GM-CSF对软脑膜侧支生长的影响尚未确定。我们检查了单侧颈总动脉(CCA)闭塞和GM-CSF治疗对小鼠软脑膜侧支生长的影响。方法:成年小鼠接受单侧CCA闭塞或假手术,然后隔日注射GM-CSF(20 g/kg)或盐水。在第7天,在1组小鼠中进行乳胶灌注以使软脑膜血管可视化,并对脑背表面上的Mac-2+单核细胞/巨噬细胞的数量进行计数。在另一组小鼠中,在第7天,进行永久性同侧大脑中动脉(MCA)闭塞,并测量梗死体积。结果:CCA闭塞后,观察到软脑膜侧支生长,GM-CSF治疗可促进侧支生长。CCA闭塞后,大脑表面Mac-2+细胞数量增加,并通过GM-CSF治疗增强。CCA闭塞后7天,GM-CSF治疗可减少随后MCA闭塞引起的梗死面积。结论:CCA闭塞后,GM-CSF治疗增强了小鼠MCA闭塞后软脑膜侧支的生长并减小了梗死面积。
Background and Purpose— Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been reported to accelerate collateral growth (arteriogenesis) at the circle of Willis in rat brain. However, the effect of GM-CSF on leptomeningeal collateral growth has not been established. We examined the effect of unilateral common carotid artery (CCA) occlusion and GM-CSF treatment on leptomeningeal collateral growth in mice. Methods— Adult mice were subjected to unilateral CCA occlusion or sham surgery followed by an alternate-day regimen of GM-CSF (20 g/kg) or saline injection. On day 7, latex perfusion was performed in 1 set of mice to visualize the leptomeningeal vessels, and the number of Mac-2+ monocytes/macrophages on the dorsal surface of the brain was counted. In another set of mice, on day 7, permanent ipsilateral middle cerebral artery (MCA) occlusion was performed, and infarct volume was measured. Results— Leptomeningeal collateral growth was observed after CCA occlusion, and that was enhanced by GM-CSF treatment. An increase in the number of Mac-2+ cells on the surface of the brain occurred after CCA occlusion and was enhanced by GM-CSF treatment. Seven days after CCA occlusion, GM-CSF treatment decreased the infarct size attributable to subsequent MCA occlusion. Conclusion— After CCA occlusion, GM-CSF treatment enhanced leptomeningeal collateral growth and decreased the infarct size after MCA occlusion in mice.