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dc.contributor.authorLi, Yuchuan
dc.contributor.authorTorp, May-Kristin
dc.contributor.authorNorheim, Frode
dc.contributor.authorKhanal, Prabhat
dc.contributor.authorKimmel, Alan R.
dc.contributor.authorStensløkken, Kåre-Olav
dc.contributor.authorVaage, Ingvar Jarle
dc.contributor.authorDalen, Knut Tomas
dc.identifier.citationLi, Y., Torp, M.-K., Norheim, F., Khanal, P., Kimmel, A. R., Stensløkken, K.-O., Vaage, J. & Dalen, K. T. (2021). Isolated Plin5-deficient cardiomyocytes store less lipid droplets than normal, but without increased sensitivity to hypoxia. Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids, 1866(4): 158873. doi:en_US
dc.description.abstractPlin5 is abundantly expressed in the heart where it binds to lipid droplets (LDs) and facilitates physical interaction between LDs and mitochondria. We isolated cardiomyocytes from adult Plin5+/+ and Plin5-/- mice to study the role of Plin5 for fatty acid uptake, LD accumulation, fatty acid oxidation, and tolerance to hypoxia. Cardiomyocytes isolated from Plin5-/- mice cultured with oleic acid stored less LDs than Plin5+/+, but comparable levels to Plin5+/+ cardiomyocytes when adipose triglyceride lipase activity was inhibited. The ability to oxidize fatty acids into CO2 was similar between Plin5+/+ and Plin5-/- cardiomyocytes, but Plin5-/- cardiomyocytes had a transient increase in intracellular fatty acid oxidation intermediates. After pre-incubation with oleic acids, Plin5-/- cardiomyocytes retained a higher content of glycogen and showed improved tolerance to hypoxia compared to Plin5+/+. In isolated, perfused hearts, deletion of Plin5 had no important effect on ventricular pressures or infarct size after ischemia. Old Plin5-/- mice had reduced levels of cardiac triacylglycerides, increased heart weight, and apart from modest elevated expression of mRNAs for beta myosin heavy chain Myh7 and the fatty acid transporter Cd36, other genes involved in fatty acid oxidation, glycogen metabolism and glucose utilization were essentially unchanged by removal of Plin5. Plin5 seems to facilitate cardiac LD storage primarily by repressing adipose triglyceride lipase activity without altering cardiac fatty acid oxidation capacity. Expression of Plin5 and cardiac LD content of isolated cardiomyocytes has little importance for tolerance to acute hypoxia and ischemia, which contrasts the protective role for Plin5 in mouse models during myocardial ischemia.en_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleIsolated Plin5-deficient cardiomyocytes store less lipid droplets than normal, but without increased sensitivity to hypoxiaen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.rights.holder© 2021 The Author(s)en_US
dc.subject.nsiVDP::Matematikk og Naturvitenskap: 400::Basale biofag: 470::Molekylærbiologi: 473en_US
dc.subject.nsiVDP::Matematikk og Naturvitenskap: 400::Zoologiske og botaniske fag: 480::Zoofysiologi og komparativ fysiologi: 483en_US
dc.subject.nsiVDP::Matematikk og Naturvitenskap: 400::Basale biofag: 470::Genetikk og genomikk: 474en_US
dc.subject.nsiVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Kardiologi: 771en_US
dc.source.journalBiochimica et Biophysica Acta - Molecular and Cell Biology of Lipidsen_US
dc.description.localcodePaid Open Accessen_US

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Navngivelse 4.0 Internasjonal
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