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Int J Biochem Cell Biol. 2017 Oct;91(Pt A):9-13. doi: 10.1016/j.biocel.2017.07.021. Epub 2017 Aug 12.

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

Author information

1
Department of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
2
Norwegian Transgenic Center, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
3
Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
4
Department of Clinical Chemistry, University of Gothenburg, Gothenburg, Sweden.
5
Atherosclerosis Research Unit, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
6
Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
7
Department of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden. Electronic address: malin.levin@wlab.gu.se.

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.

KEYWORDS:

Cardiomyocyte; Lipid droplet protein; Mitochondria; Oxidative capacity; Perilipin5

PMID:
28811250
DOI:
10.1016/j.biocel.2017.07.021
[Indexed for MEDLINE]

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