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Plin2-deficiency reduces lipophagy and results in increased lipid accumulation in the heart.

Journal article
Authors Ismena Mardani
Dalen Knut Tomas
Christina Drevinge
Azra Miljanovic
Marcus Ståhlman
Martina Klevstig
Margareta Scharin Täng
Per Fogelstrand
Max Levin
Matias Ekstrand
Syam Nair
Björn Redfors
Elmir Omerovic
Linda Andersson
Kimmel Alan R
Jan Borén
Malin Levin
Published in Scientific reports
Volume 9
Issue 1
ISSN 2045-2322
Publication year 2019
Published at Wallenberg Laboratory
Institute of Neuroscience and Physiology
Institute of Medicine, Department of Molecular and Clinical Medicine
Language en
Links dx.doi.org/10.1038/s41598-019-43335...
www.ncbi.nlm.nih.gov/entrez/query.f...
Subject categories Cardiovascular medicine

Abstract

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.

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