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Deficiency in perilipin 5 reduces mitochondrial function and membrane depolarization in mouse hearts.

Journal article
Authors Linda Andersson
Christina Drevinge
Ismena Mardani
Knut T Dalen
Marcus Ståhlman
Martina Klevstig
Annika Lundqvist
Fred Haugen
Martin Adiels
Per Fogelstrand
Jorge Asin-Cayuela
Lillemor Mattsson Hultén
Max Levin
Ewa Ehrenborg
Yun K Lee
Alan R Kimmel
Jan Borén
Malin Levin
Published in The international journal of biochemistry & cell biology
Volume 91
Issue Pt A
Pages 9-13
ISSN 1878-5875
Publication year 2017
Published at Wallenberg Laboratory
Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 9-13
Language en
Links dx.doi.org/10.1016/j.biocel.2017.07...
www.ncbi.nlm.nih.gov/entrez/query.f...
Subject categories Cancer and Oncology

Abstract

Myocardial triglycerides stored in lipid droplets are important in regulating the intracellular delivery of fatty acids for energy generation in mitochondria, for membrane biosynthesis, and as agonists for intracellular signaling. Previously, we showed that deficiency in the lipid droplet protein perilipin 5 (Plin5) markedly reduces triglyceride storage in cardiomyocytes and increases the flux of fatty acids into phospholipids. Here, we investigated whether Plin5 deficiency in cardiomyocytes alters mitochondrial function. We found that Plin5 deficiency reduced mitochondrial oxidative capacity. Furthermore, in mitochondria from Plin5((-/)(-)) hearts, the fatty acyl composition of phospholipids in mitochondrial membranes was altered and mitochondrial membrane depolarization was markedly compromised. These findings suggest that mitochondria isolated from hearts deficient in Plin5, have specific functional defects.

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