Deficiency in perilipin 5 reduces mitochondrial function and membrane depolarization in mouse hearts
Deficiency in perilipin 5 reduces mitochondrial function and membrane depolarization in mouse hearts
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DOI：
10.1016/j.biocel.2017.07.021
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发表时间：
2017-10-01
影响因子：
4
通讯作者：
Levin, Malin C.
中科院分区：
文献类型：
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作者：
Andersson, Linda;Drevinge, Christina;Levin, Malin C.
储存在脂滴中的心肌甘油三酯在调节脂肪酸的细胞内递送、线粒体能量生成、膜生物合成以及作为细胞内信号传导的激动剂方面具有重要作用。先前，我们发现脂滴蛋白perilippin 5 （Plin5）的缺乏显著降低了心肌细胞中甘油三酯的储存，并增加了脂肪酸进入磷脂的通量。在这里，我们研究了心肌细胞Plin5缺乏是否会改变线粒体功能。我们发现Pli5缺陷降低了线粒体氧化能力。此外，在来自Plin5（-/-）心脏的线粒体中，线粒体膜磷脂的脂肪酰基组成被改变，线粒体膜去极化明显受损。这些发现表明，从缺乏Plin5的心脏中分离的线粒体具有特定的功能缺陷。
Myocardial triglycerides stored in lipid droplets are important in regulating the intracellular delivery of fatty acids for energy generation in mitochondria, for membrane biosynthesis, and as agonists for intracellular signaling. Previously, we showed that deficiency in the lipid droplet protein perilipin 5 (Plin5) markedly reduces triglyceride storage in cardiomyocytes and increases the flux of fatty acids into phospholipids. Here, we investigated whether Plin5 deficiency in cardiomyocytes alters mitochondrial function. We found that Pli5 deficiency reduced mitochondrial oxidative capacity. Furthermore, in mitochondria from Plin5(-/-) hearts, the fatty acyl composition of phospholipids in mitochondrial membranes was altered and mitochondrial membrane de-polarization was markedly compromised. These findings suggest that mitochondria isolated from hearts deficient in Plin5, have specific functional defects.