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PPAR Research
Volume 2011 (2011), Article ID 372854, 13 pages
Research Article

Cardiomyocyte-Restricted Deletion of PPARβ/δ in PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation

1Department of Nutrition Sciences, University of Alabama at Birmingham, 1675 University Boulevard, Birmingham, AL 35294-3360, USA
2Department of Anatomy, Second Military Medical University, Shanghai 200433, China
3Department of Cardio Thoracic Surgery, Hunan Children’s Hospital, Changsha 410007, China
4Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA 30322, USA
5Department of Anatomy, Morehouse School of Medicine, Atlanta, GA 30310, USA
6Department of Pathology, Emory University, Atlanta, GA 30322, USA

Received 30 April 2011; Revised 27 June 2011; Accepted 28 June 2011

Academic Editor: Brian Finck

Copyright © 2011 Jian Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Supplemental file 1: A table contains information of primers used in Real Time PCR experiments to detect transcript expression levels.

Supplemental File 2: Supplemental figures demonstrate changes in mitochondrial volume and DNA copy number: The mitochondrial volume was quantified based on electron micrographs of α-MyHC-Cre, PPARα-/- , CR-PPARβ/δ -/- , CR-Pd/Pa null heart sections. Mitochondrial DNA copy number was measured by Real time PCR.

  1. Supplementary Material
  2. Supplementary Material