NDLI: G0/G1 Switch Gene 2 Regulates Cardiac Lipolysis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Schmidt, Albrecht Heier, Christoph Schreiber, Renate Grond, Susanne Zimmermann, Robert Radner, Franz P. W. Schweiger, Martina Moustafa, Tarek Cerk, Ines K. Wojciechowski, Jacek Theussl, H-christian Penninger, Josef M. Eichmann, Thomas O. Zechner, Rudolf Oberer, Monika
Description	Author Affiliation: Heier C ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria.); Radner FP ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria.); Moustafa T ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria, the Laboratory of Experimental and Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Internal Medicine and.); Schreiber R ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria.); Grond S ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria.); Eichmann TO ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria.); Schweiger M ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria.); Schmidt A ( Division of Cardiology, Department of Internal Medicine, Medical University of Graz, A-8036 Graz, Austria, and.); Cerk IK ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria.); Oberer M ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria.); Theussl HC ( the Transgenic Service, Research Institute of Molecular Pathology (IMP), 1030 Vienna, Austria, and the IMBA Institute of Molecular Biotechnology of the Austrian Academy of Sciences, 1030 Vienna, Austria.); Wojciechowski J ( the Transgenic Service, Research Institute of Molecular Pathology (IMP), 1030 Vienna, Austria, and the IMBA Institute of Molecular Biotechnology of the Austrian Academy of Sciences, 1030 Vienna, Austria.); Penninger JM ( the Transgenic Service, Research Institute of Molecular Pathology (IMP), 1030 Vienna, Austria, and the IMBA Institute of Molecular Biotechnology of the Austrian Academy of Sciences, 1030 Vienna, Austria.); Zimmermann R ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria.); Zechner R ( From the Institute of Molecular Biosciences, University of Graz, A-8010 Graz, Austria, rudolf.zechner@uni-graz.at.)
Abstract	The anabolism and catabolism of myocardial triacylglycerol (TAG) stores are important processes for normal cardiac function. TAG synthesis detoxifies and stockpiles fatty acids to prevent lipotoxicity, whereas TAG hydrolysis (lipolysis) remobilizes fatty acids from endogenous storage pools as energy substrates, signaling molecules, or precursors for complex lipids. This study focused on the role of G0/G1 switch 2 (G0S2) protein, which was previously shown to inhibit the principal TAG hydrolase adipose triglyceride lipase (ATGL), in the regulation of cardiac lipolysis. Using wild-type and mutant mice, we show the following: (i) G0S2 is expressed in the heart and regulated by the nutritional status with highest expression levels after re-feeding. (ii) Cardiac-specific overexpression of G0S2 inhibits cardiac lipolysis by direct protein-protein interaction with ATGL. This leads to severe cardiac steatosis. The steatotic hearts caused by G0S2 overexpression are less prone to fibrotic remodeling or cardiac dysfunction than hearts with a lipolytic defect due to ATGL deficiency. (iii) Conversely to the phenotype of transgenic mice, G0S2 deficiency results in a de-repression of cardiac lipolysis and decreased cardiac TAG content. We conclude that G0S2 acts as a potent ATGL inhibitor in the heart modulating cardiac substrate utilization by regulating cardiac lipolysis.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	43
Volume Number	290
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2015-10-23
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Cycle Proteins Genetics G1 Phase Lipolysis Myocardium Metabolism G0 Phase Triglycerides Animals Cell Line Heart Function Tests Mice Mice, Inbred C57BL Mice, Transgenic Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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