Plin2-deficiency reduces lipophagy and results in increased lipid accumulation in the heart
Identifieur interne : 000597 ( Ncbi/Curation ); précédent : 000596; suivant : 000598Plin2-deficiency reduces lipophagy and results in increased lipid accumulation in the heart
Auteurs : Ismena Mardani [Suède] ; Knut Tomas Dalen [Norvège] ; Christina Drevinge [Suède] ; Azra Miljanovic [Suède] ; Marcus St Hlman [Suède] ; Martina Klevstig [Suède] ; Margareta Scharin T Ng [Suède] ; Per Fogelstrand [Suède] ; Max Levin [Suède] ; Matias Ekstrand [Suède] ; Syam Nair [Suède] ; Björn Redfors [Suède] ; Elmir Omerovic [Suède] ; Linda Andersson [Suède] ; Alan R. Kimmel [États-Unis] ; Jan Borén [Suède] ; Malin C. Levin [Suède]Source :
- Scientific Reports [ 2045-2322 ] ; 2019.
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
Url:
DOI: 10.1038/s41598-019-43335-y
PubMed: 31061399
PubMed Central: 6502866
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PMC:6502866Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Plin2-deficiency reduces lipophagy and results in increased lipid accumulation in the heart</title>
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Gothenburg, Sweden</nlm:aff>
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<wicri:regionArea>Gothenburg</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Redfors, Bjorn" sort="Redfors, Bjorn" uniqKey="Redfors B" first="Björn" last="Redfors">Björn Redfors</name>
<affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">000000009445082X</institution-id>
<institution-id institution-id-type="GRID">grid.1649.a</institution-id>
<institution>Department of Molecular and Clinical Medicine/Wallenberg Laboratory,</institution>
<institution>Institute of Medicine, the Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital,</institution>
</institution-wrap>
Gothenburg, Sweden</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Gothenburg</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Omerovic, Elmir" sort="Omerovic, Elmir" uniqKey="Omerovic E" first="Elmir" last="Omerovic">Elmir Omerovic</name>
<affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">000000009445082X</institution-id>
<institution-id institution-id-type="GRID">grid.1649.a</institution-id>
<institution>Department of Molecular and Clinical Medicine/Wallenberg Laboratory,</institution>
<institution>Institute of Medicine, the Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital,</institution>
</institution-wrap>
Gothenburg, Sweden</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Gothenburg</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Andersson, Linda" sort="Andersson, Linda" uniqKey="Andersson L" first="Linda" last="Andersson">Linda Andersson</name>
<affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">000000009445082X</institution-id>
<institution-id institution-id-type="GRID">grid.1649.a</institution-id>
<institution>Department of Molecular and Clinical Medicine/Wallenberg Laboratory,</institution>
<institution>Institute of Medicine, the Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital,</institution>
</institution-wrap>
Gothenburg, Sweden</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Gothenburg</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Kimmel, Alan R" sort="Kimmel, Alan R" uniqKey="Kimmel A" first="Alan R." last="Kimmel">Alan R. Kimmel</name>
<affiliation wicri:level="2"><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2297 5165</institution-id>
<institution-id institution-id-type="GRID">grid.94365.3d</institution-id>
<institution>Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases,</institution>
<institution>National Institutes of Health,</institution>
</institution-wrap>
Bethesda, MD USA</nlm:aff>
<country>États-Unis</country>
<placeName><region type="state">Maryland</region>
</placeName>
<wicri:cityArea>Bethesda</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Boren, Jan" sort="Boren, Jan" uniqKey="Boren J" first="Jan" last="Borén">Jan Borén</name>
<affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">000000009445082X</institution-id>
<institution-id institution-id-type="GRID">grid.1649.a</institution-id>
<institution>Department of Molecular and Clinical Medicine/Wallenberg Laboratory,</institution>
<institution>Institute of Medicine, the Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital,</institution>
</institution-wrap>
Gothenburg, Sweden</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Gothenburg</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Levin, Malin C" sort="Levin, Malin C" uniqKey="Levin M" first="Malin C." last="Levin">Malin C. Levin</name>
<affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">000000009445082X</institution-id>
<institution-id institution-id-type="GRID">grid.1649.a</institution-id>
<institution>Department of Molecular and Clinical Medicine/Wallenberg Laboratory,</institution>
<institution>Institute of Medicine, the Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital,</institution>
</institution-wrap>
Gothenburg, Sweden</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Gothenburg</wicri:regionArea>
</affiliation>
</author>
</analytic>
<series><title level="j">Scientific Reports</title>
<idno type="eISSN">2045-2322</idno>
<imprint><date when="2019">2019</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p id="Par1">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 <italic>Plin2</italic>
<sup>−/−</sup>
mice. Although <italic>Plin2</italic>
<sup>−/−</sup>
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 <italic>Plin2</italic>
<sup>−/−</sup>
mice compared with <italic>Plin2</italic>
<sup>+/+</sup>
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.</p>
</div>
</front>
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