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在小鼠中,帕金介导的线粒细胞衰老指导了周产期心脏代谢成熟

Guohua Gong¹, Moshi Song¹, Gyorgy Csordas²

¹Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA.

Science (New York, N.Y.)

|January 20, 2016

概括

帕金介导的线粒体除胎儿线粒体,使成熟的成人线粒体能够在周围心脏中发育. 这一过程对于心脏代谢适应和生存至关重要.

科学领域:

心血管生物学
线粒体生物学
发育生物学

背景情况:

发育中的心脏从碳水化合物转移到脂肪酸代谢.
驱动这种线粒体可塑性的机制尚未完全理解.

研究的目的:

调查PINK1-Mfn2-Parkin介导的线粒细胞在周围心脏代谢重编程中的作用.
阐明心脏发育中的线粒体可塑性背后的机制.

主要方法:

使用了一种具有缺少PINK1化位点 (Mfn2AA) 的线粒素 (Mfn) 2突变的小鼠模型.
检查心脏帕金删除和Mfn2AA表达从出生与断奶后.
在新生儿和成年小鼠心脏中评估线粒体功能,基因表达和代谢特征.

主要成果:

在不影响线粒体融合的情况下,Mfn2 AA突变抑制了帕金转位和线粒体融合.
心脏帕金缺失或Mfn2AA表达从出生后受损的线粒体成熟和生存.
Mfn2 AA心脏显示出胎儿线粒体转录特征,脂肪酸代谢减少,心肌细胞呼吸抑制.

结论:

围产期帕金介导的线粒细胞和成熟线粒体的替代,而不是转录重编程,驱动心脏代谢过渡.
对于心肌细胞发育中的线粒体可塑性和围产期心脏代谢适应,线粒体的去除是必不可少的.

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