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粒细胞集落刺激因子不会增强急性心肌梗死大鼠骨髓来源细胞的募集。

Granulocyte colony-stimulating factor does not enhance recruitment of bone marrow-derived cells in rats with acute myocardial infarction.

作者信息

Sato Daisuke, Otani Hajime, Fujita Masanori, Shimazu Takayuki, Yoshioka Kei, Enoki Chiharu, Minato Naoki, Iwasaka Toshiji

机构信息

Second Department of Internal Medicine;

出版信息

Exp Clin Cardiol. 2012 Sep;17(3):83-8.

Abstract

Despite the potential benefit of granulocyte colony-stimulating factor (G-CSF) therapy in patients with acute myocardial infarction (MI), the efficacy of G-CSF in regenerating the heart after MI remains controversial. The authors hypothesize that the limited efficacy of G-CSF is related to its inhibitory effect on recruitment of bone marrow-derived cells (BMCs) to the infarcted tissue. MI was induced in rats with intrabone marrow-bone marrow transplantation from syngenic rats expressing green fluorescence protein to track BMCs. G-CSF was administered for five days after the onset of MI. G-CSF increased the number of CD45(+) cells in the peripheral circulation but did not increase their recruitment to the heart. G-CSF had no effect on myocardial stromal-derived factor-1 alpha and chemokine (C-X-C motif) receptor 4 (CXCR4) expression in mononuclear cells in the peripheral blood and CXCR4(+) cells in the heart. G-CSF had no effect on angiogenesis, myocardial fibrosis or left ventricular function four weeks after MI. These results suggest that G-CSF mobilizes BMCs to the peripheral circulation but does not increase recruitment to the infarcted myocardium despite preservation of the stromal-derived factor-1 alpha/CXCR4 axis.

摘要

尽管粒细胞集落刺激因子(G-CSF)疗法对急性心肌梗死(MI)患者具有潜在益处,但G-CSF在MI后心脏再生中的疗效仍存在争议。作者推测,G-CSF疗效有限与其对骨髓源性细胞(BMCs)募集至梗死组织的抑制作用有关。通过将表达绿色荧光蛋白的同基因大鼠进行骨髓内骨髓移植,在大鼠中诱导MI以追踪BMCs。MI发作后给予G-CSF五天。G-CSF增加了外周循环中CD45(+)细胞的数量,但并未增加其向心脏的募集。G-CSF对外周血单核细胞中的心肌基质衍生因子-1α和趋化因子(C-X-C基序)受体4(CXCR4)表达以及心脏中的CXCR4(+)细胞没有影响。MI四周后,G-CSF对血管生成、心肌纤维化或左心室功能没有影响。这些结果表明,G-CSF可将BMCs动员至外周循环,但尽管保留了基质衍生因子-1α/CXCR4轴,却并未增加其向梗死心肌的募集。

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