Plin2-deficiency reduces lipophagy and results in increased lipid accumulation in the heart
Identifieur interne : 000485 ( Pmc/Checkpoint ); précédent : 000484; suivant : 000486Plin2-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
Affiliations:
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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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<author><name sortKey="Omerovic, Elmir" sort="Omerovic, Elmir" uniqKey="Omerovic E" first="Elmir" last="Omerovic">Elmir Omerovic</name>
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Gothenburg, Sweden</nlm:aff>
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<author><name sortKey="Andersson, Linda" sort="Andersson, Linda" uniqKey="Andersson L" first="Linda" last="Andersson">Linda Andersson</name>
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Gothenburg, Sweden</nlm:aff>
<country xml:lang="fr">Suède</country>
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<author><name sortKey="Kimmel, Alan R" sort="Kimmel, Alan R" uniqKey="Kimmel A" first="Alan R." last="Kimmel">Alan R. Kimmel</name>
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Bethesda, MD USA</nlm:aff>
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<author><name sortKey="Boren, Jan" sort="Boren, Jan" uniqKey="Boren J" first="Jan" last="Borén">Jan Borén</name>
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Gothenburg, Sweden</nlm:aff>
<country xml:lang="fr">Suède</country>
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<author><name sortKey="Levin, Malin C" sort="Levin, Malin C" uniqKey="Levin M" first="Malin C." last="Levin">Malin C. Levin</name>
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<institution-id institution-id-type="GRID">grid.1649.a</institution-id>
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Gothenburg, Sweden</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Gothenburg</wicri:regionArea>
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</analytic>
<series><title level="j">Scientific Reports</title>
<idno type="eISSN">2045-2322</idno>
<imprint><date when="2019">2019</date>
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<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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<front><journal-meta><journal-id journal-id-type="nlm-ta">Sci Rep</journal-id>
<journal-id journal-id-type="iso-abbrev">Sci Rep</journal-id>
<journal-title-group><journal-title>Scientific Reports</journal-title>
</journal-title-group>
<issn pub-type="epub">2045-2322</issn>
<publisher><publisher-name>Nature Publishing Group UK</publisher-name>
<publisher-loc>London</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31061399</article-id>
<article-id pub-id-type="pmc">6502866</article-id>
<article-id pub-id-type="publisher-id">43335</article-id>
<article-id pub-id-type="doi">10.1038/s41598-019-43335-y</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Plin2-deficiency reduces lipophagy and results in increased lipid accumulation in the heart</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Mardani</surname>
<given-names>Ismena</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tomas Dalen</surname>
<given-names>Knut</given-names>
</name>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Drevinge</surname>
<given-names>Christina</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Miljanovic</surname>
<given-names>Azra</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ståhlman</surname>
<given-names>Marcus</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Klevstig</surname>
<given-names>Martina</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Scharin Täng</surname>
<given-names>Margareta</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Fogelstrand</surname>
<given-names>Per</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Levin</surname>
<given-names>Max</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid">http://orcid.org/0000-0002-0403-9266</contrib-id>
<name><surname>Ekstrand</surname>
<given-names>Matias</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nair</surname>
<given-names>Syam</given-names>
</name>
<xref ref-type="aff" rid="Aff3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Redfors</surname>
<given-names>Björn</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Omerovic</surname>
<given-names>Elmir</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Andersson</surname>
<given-names>Linda</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kimmel</surname>
<given-names>Alan R.</given-names>
</name>
<xref ref-type="aff" rid="Aff4">4</xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid">http://orcid.org/0000-0003-0786-8091</contrib-id>
<name><surname>Borén</surname>
<given-names>Jan</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Levin</surname>
<given-names>Malin C.</given-names>
</name>
<address><email>malin.levin@wlab.gu.se</email>
</address>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<aff id="Aff1"><label>1</label>
<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</aff>
<aff id="Aff2"><label>2</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1936 8921</institution-id>
<institution-id institution-id-type="GRID">grid.5510.1</institution-id>
<institution>Department of Nutrition, Institute of Basic Medical Sciences,</institution>
<institution>University of Oslo,</institution>
</institution-wrap>
Oslo, Norway</aff>
<aff id="Aff3"><label>3</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0000 9919 9582</institution-id>
<institution-id institution-id-type="GRID">grid.8761.8</institution-id>
<institution>Centre of Perinatal Medicine and Health, Institute of Neuroscience and Physiology,</institution>
<institution>The Sahlgrenska Academy at University of Gothenburg,</institution>
</institution-wrap>
Gothenburg, Sweden</aff>
<aff id="Aff4"><label>4</label>
<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</aff>
</contrib-group>
<pub-date pub-type="epub"><day>6</day>
<month>5</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>6</day>
<month>5</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>9</volume>
<elocation-id>6909</elocation-id>
<history><date date-type="received"><day>25</day>
<month>10</month>
<year>2018</year>
</date>
<date date-type="accepted"><day>23</day>
<month>4</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© The Author(s) 2019</copyright-statement>
<license license-type="OpenAccess"><license-p><bold>Open Access</bold>
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>
.</license-p>
</license>
</permissions>
<abstract id="Abs1"><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>
</abstract>
<kwd-group kwd-group-type="npg-subject"><title>Subject terms</title>
<kwd>Molecular biology</kwd>
<kwd>Molecular medicine</kwd>
</kwd-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/501100004359</institution-id>
<institution>Vetenskapsrådet (Swedish Research Council)</institution>
</institution-wrap>
</funding-source>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/501100003793</institution-id>
<institution>Hjärt-Lungfonden (Swedish Heart-Lung Foundation)</institution>
</institution-wrap>
</funding-source>
</award-group>
</funding-group>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© The Author(s) 2019</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>Norvège</li>
<li>Suède</li>
<li>États-Unis</li>
</country>
<region><li>Maryland</li>
</region>
</list>
<tree><country name="Suède"><noRegion><name sortKey="Mardani, Ismena" sort="Mardani, Ismena" uniqKey="Mardani I" first="Ismena" last="Mardani">Ismena Mardani</name>
</noRegion>
<name sortKey="Andersson, Linda" sort="Andersson, Linda" uniqKey="Andersson L" first="Linda" last="Andersson">Linda Andersson</name>
<name sortKey="Boren, Jan" sort="Boren, Jan" uniqKey="Boren J" first="Jan" last="Borén">Jan Borén</name>
<name sortKey="Drevinge, Christina" sort="Drevinge, Christina" uniqKey="Drevinge C" first="Christina" last="Drevinge">Christina Drevinge</name>
<name sortKey="Ekstrand, Matias" sort="Ekstrand, Matias" uniqKey="Ekstrand M" first="Matias" last="Ekstrand">Matias Ekstrand</name>
<name sortKey="Fogelstrand, Per" sort="Fogelstrand, Per" uniqKey="Fogelstrand P" first="Per" last="Fogelstrand">Per Fogelstrand</name>
<name sortKey="Klevstig, Martina" sort="Klevstig, Martina" uniqKey="Klevstig M" first="Martina" last="Klevstig">Martina Klevstig</name>
<name sortKey="Levin, Malin C" sort="Levin, Malin C" uniqKey="Levin M" first="Malin C." last="Levin">Malin C. Levin</name>
<name sortKey="Levin, Max" sort="Levin, Max" uniqKey="Levin M" first="Max" last="Levin">Max Levin</name>
<name sortKey="Miljanovic, Azra" sort="Miljanovic, Azra" uniqKey="Miljanovic A" first="Azra" last="Miljanovic">Azra Miljanovic</name>
<name sortKey="Nair, Syam" sort="Nair, Syam" uniqKey="Nair S" first="Syam" last="Nair">Syam Nair</name>
<name sortKey="Omerovic, Elmir" sort="Omerovic, Elmir" uniqKey="Omerovic E" first="Elmir" last="Omerovic">Elmir Omerovic</name>
<name sortKey="Redfors, Bjorn" sort="Redfors, Bjorn" uniqKey="Redfors B" first="Björn" last="Redfors">Björn Redfors</name>
<name sortKey="Scharin T Ng, Margareta" sort="Scharin T Ng, Margareta" uniqKey="Scharin T Ng M" first="Margareta" last="Scharin T Ng">Margareta Scharin T Ng</name>
<name sortKey="St Hlman, Marcus" sort="St Hlman, Marcus" uniqKey="St Hlman M" first="Marcus" last="St Hlman">Marcus St Hlman</name>
</country>
<country name="Norvège"><noRegion><name sortKey="Tomas Dalen, Knut" sort="Tomas Dalen, Knut" uniqKey="Tomas Dalen K" first="Knut" last="Tomas Dalen">Knut Tomas Dalen</name>
</noRegion>
</country>
<country name="États-Unis"><region name="Maryland"><name sortKey="Kimmel, Alan R" sort="Kimmel, Alan R" uniqKey="Kimmel A" first="Alan R." last="Kimmel">Alan R. Kimmel</name>
</region>
</country>
</tree>
</affiliations>
</record>
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