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在急性心肌梗塞后减少白细胞的产生

Hendrik B Sager¹, Timo Heidt¹, Maarten Hulsmans¹

¹From Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, Boston, MA (H.B.S., T.H., M.H., P.D., G.C., M.S., G.R.W., B.T., Y.I., Y.S., R.W., F.K.S., M.N.); Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.); and Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (P.L.).

|September 12, 2015

概括

在心肌梗塞 (MI) 后,介质素-1β信号增加了造血干细胞的增殖,导致白细胞的增加. 阻断这种信号可以减少心脏病发作后的炎症和心力衰竭.

科学领域:

免疫学
血液学
心血管科学

背景情况:

心肌梗塞 (MI) 是一种导致白细胞大量增加的缺血性损伤.
心脏病发作后血白细胞数量升高与患者的存活率降低有关.
在MI后导致白细胞产量增加的特定信号尚未完全理解.

研究的目的:

研究心肌梗塞刺激骨髓造血干细胞增殖的机制.
识别与MI后白细胞形成有关的关键分子信号.
评估针对这些信号的治疗潜力,以减轻不良的心脏重塑和心力衰竭.

主要方法:

为了评估系统信号,
骨髓复合实验以评估造血干细胞的行为.
在体内给予抗素-1β抗体.
在患有动脉样硬化的ApoE-/ -小鼠中评估白细胞数量,炎症和心脏功能.

主要成果:

包括IL-1β在内的可溶性危险信号被确定为MI后造血干细胞增殖的驱动因素.
IL- 1β直接作用于造血细胞并调节骨髓微环境以增强增殖.
用抗体中和IL- 1β抑制了MI后的造血干细胞增殖.
在小鼠模型中,抗IL- 1β治疗降低了血液和心脏病组织中的白细胞数量,从而减少了炎症和心脏病发作后心力衰竭.

结论:

骨髓激活是通过IL-1β等信号进行的.
向IL-1β是一种减少受损心脏炎症的潜在治疗策略.
调节骨髓对心脏病的反应可能会影响心脏病的结果和心力衰竭的进展.

关键词:

血液形成造血干细胞抗胰岛素的治疗方法心肌梗塞

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