Wnt5a介导的中性粒细胞招募在压力过载引起的心脏功能障碍中具有强制性的作用
Ying Wang1,2, Soichi Sano1, Kosei Oshima3
1Hematovascular Biology Center, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville (Y. Wang, S.S., M.S., Y.Y., C.J., K.W.).
Circulation
|June 8, 2019
概括
中性粒细胞在压力过度引起的心力衰竭中起着关键作用. Wnt5a信号调节中性粒细胞透,影响心脏缩和功能.
科学领域:
- 心脏病学
- 免疫学
- 分子生物学
背景情况:
- 已知巨细胞在心肌损伤中的作用,但对非缺血性心脏病理中的中性粒细胞的研究不足.
- 对于了解心力衰竭来说,研究压力过载引起的心脏缩中的中性粒细胞功能至关重要.
研究的目的:
- 阐明中性粒细胞在压力过度诱导的心脏缩中的作用和调节.
- 确定Wnt5a信号的参与中性粒细胞透和心脏病理.
主要方法:
- 用Ly6G抗体治疗小鼠以减少中性粒细胞.
- 在小鼠中进行横向大动脉收缩 (TAC),以诱导压力过载.
- 在骨髓细胞中操纵了Wnt5a表达 (缺乏或过度表达).
主要成果:
- 中性粒细胞消耗减轻了TAC引起的心脏缩,炎症,并保持了心脏功能.
- 骨髓Wnt5a缺乏抑制了中性粒细胞的透,并模仿了中性粒细胞衰竭的作用.
- 骨髓细胞中的Wnt5a过度表达加剧了心脏缩,炎症和功能障碍.
结论:
- 在压力过载引起的心力衰竭中,Wnt5a调节的中性粒细胞透至关重要.
- 向中性粒细胞透可能为心脏缩和心力衰竭提供治疗策略.
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