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Plin2-deficiency reduces lipophagy and results in increased lipid accumulation in the heart.
Scientific Reports ( IF 3.8 ) Pub Date : 2019-05-06 , DOI: 10.1038/s41598-019-43335-y
Ismena Mardani 1 , Knut Tomas Dalen 2 , Christina Drevinge 1 , Azra Miljanovic 1 , Marcus Ståhlman 1 , Martina Klevstig 1 , Margareta Scharin Täng 1 , Per Fogelstrand 1 , Max Levin 1 , Matias Ekstrand 1 , Syam Nair 3 , Björn Redfors 1 , Elmir Omerovic 1 , Linda Andersson 1 , Alan R Kimmel 4 , Jan Borén 1 , Malin C Levin 1
Scientific Reports ( IF 3.8 ) Pub Date : 2019-05-06 , DOI: 10.1038/s41598-019-43335-y
Ismena Mardani 1 , Knut Tomas Dalen 2 , Christina Drevinge 1 , Azra Miljanovic 1 , Marcus Ståhlman 1 , Martina Klevstig 1 , Margareta Scharin Täng 1 , Per Fogelstrand 1 , Max Levin 1 , Matias Ekstrand 1 , Syam Nair 3 , Björn Redfors 1 , Elmir Omerovic 1 , Linda Andersson 1 , Alan R Kimmel 4 , Jan Borén 1 , Malin C Levin 1
Affiliation
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Myocardial dysfunction is commonly associated with accumulation of cardiac lipid droplets (LDs). Perilipin 2 (Plin2) is a LD protein that is involved in LD formation, stability and trafficking events within the cell. Even though Plin2 is highly expressed in the heart, little is known about its role in myocardial lipid storage. A recent report shows that cardiac overexpression of Plin2 result in massive myocardial steatosis suggesting that Plin2 stabilizes LDs. In this study, we hypothesized that deficiency in Plin2 would result in reduced myocardial lipid storage. In contrast to our hypothesis, we found increased accumulation of triglycerides in hearts, and specifically in cardiomyocytes, from Plin2-/- mice. Although Plin2-/- mice had markedly enhanced lipid levels in the heart, they had normal heart function under baseline conditions and under mild stress. However, after an induced myocardial infarction, stroke volume and cardiac output were reduced in Plin2-/- mice compared with Plin2+/+ mice. We further demonstrated that the increased triglyceride accumulation in Plin2-deficient hearts was caused by altered lipophagy. Together, our data show that Plin2 is important for proper hydrolysis of LDs.
中文翻译：
Plin2缺乏症会减少脂肪吞噬，并导致脂质在心脏中的积累增加。
心肌功能障碍通常与心脏脂质滴（LDs）的积累有关。Perilipin 2（Plin2）是一种LD蛋白，参与细胞内LD的形成，稳定性和运输事件。尽管Plin2在心脏中高度表达，但对其在心肌脂质存储中的作用知之甚少。最近的报告显示，Plin2的心脏过度表达会导致大量的心肌脂肪变性，这表明Plin2使LDs稳定。在这项研究中，我们假设Plin2的缺乏会导致心肌脂质储存减少。与我们的假设相反，我们发现Plin2-/-小鼠的心脏，尤其是心肌细胞中的甘油三酸酯蓄积增加。尽管Plin2-/-小鼠的心脏脂质水平显着提高，在基线状态和轻度压力下，他们的心脏功能正常。但是，在诱发心肌梗塞后，与Plin2 + / +小鼠相比，Plin2-/-小鼠的中风量和心输出量降低。我们进一步证明，在Plin2缺乏的心脏中，甘油三酸酯积累的增加是由改变的脂肪吞噬引起的。总之，我们的数据表明Plin2对于LD的正确水解非常重要。
更新日期：2019-05-06
中文翻译：
Plin2缺乏症会减少脂肪吞噬，并导致脂质在心脏中的积累增加。
心肌功能障碍通常与心脏脂质滴（LDs）的积累有关。Perilipin 2（Plin2）是一种LD蛋白，参与细胞内LD的形成，稳定性和运输事件。尽管Plin2在心脏中高度表达，但对其在心肌脂质存储中的作用知之甚少。最近的报告显示，Plin2的心脏过度表达会导致大量的心肌脂肪变性，这表明Plin2使LDs稳定。在这项研究中，我们假设Plin2的缺乏会导致心肌脂质储存减少。与我们的假设相反，我们发现Plin2-/-小鼠的心脏，尤其是心肌细胞中的甘油三酸酯蓄积增加。尽管Plin2-/-小鼠的心脏脂质水平显着提高，在基线状态和轻度压力下，他们的心脏功能正常。但是，在诱发心肌梗塞后，与Plin2 + / +小鼠相比，Plin2-/-小鼠的中风量和心输出量降低。我们进一步证明，在Plin2缺乏的心脏中，甘油三酸酯积累的增加是由改变的脂肪吞噬引起的。总之，我们的数据表明Plin2对于LD的正确水解非常重要。
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