Differential effects of chronic, in vivo, PPAR’s stimulation on the myocardial subcellular redistribution of FAT/CD36 and FABPpm

Kalinowska, Agnieszka; Górski, Jan; Harasim, Ewa; Harasiuk, Dorota; Bonen, Arend; Chabowski, Adrian

doi:10.1016/j.febslet.2009.07.008

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Volume 583, Issue 15 , Pages 2527-2534, 6 August 2009

Differential effects of chronic, in vivo, PPAR’s stimulation on the myocardial subcellular redistribution of FAT/CD36 and FABPpm

Edited by Laszlo Nagy

Agnieszka Kalinowska
- Department of Physiology, Medical University of Białystok, 15-089 Białystok, ul. Mickiewicza 2C, Poland
Jan Górski
- Department of Physiology, Medical University of Białystok, 15-089 Białystok, ul. Mickiewicza 2C, Poland
Ewa Harasim
- Department of Physiology, Medical University of Białystok, 15-089 Białystok, ul. Mickiewicza 2C, Poland
Dorota Harasiuk
- Department of Physiology, Medical University of Białystok, 15-089 Białystok, ul. Mickiewicza 2C, Poland
Arend Bonen
- Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1
Adrian Chabowski
- Department of Physiology, Medical University of Białystok, 15-089 Białystok, ul. Mickiewicza 2C, Poland
- Corresponding author. Fax: +48 085 7485585.

Received 27 January 2009; received in revised form 2 July 2009; accepted 7 July 2009. published online 13 July 2009.

Abstract

This study reveals that the activation of either PPARα (WY 14643) or PPARβ (GW0742) each induce the translocation of FAT/CD36 from an intracellular pool(s) to the plasma membrane, while PPARβ also induces the subcellular redistribution of FABPpm(Got2) to the plasma membrane. In contrast, activation of PPARγ failed to induce the subcellular redistribution of FAT/CD36 and FABPpm. These PPARα-, and PPARβ-induced changes in the plasmalemmal content of these fatty acid transporters were associated with the concurrent upregulation of fatty acid triacylglycerol esterification (PPARβ) and oxidation (PPARα and PPARβ). Observed effects of chronic PPAR stimulation were not related to either AMPK or ERK1/2 activation.