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
Figure 4
Expression of key determinants of mitochondrial biogenesis and mitochondrial proteins. (a) Real-time PCR measurement of transcript levels of NRF-1, NRF2 (a and b subunits), PGC-1α and -1β, and TFAM on samples from TMCM, PPARα −/−, TMPD, and TMPDPA hearts. (b) Western blotting analyses of relative protein levels of PGC-1α and TFAM on samples of nuclear proteins extracted from ventricular tissues of TMCM, PPARα −/−, TMPD, and TMPDPA mice. (c) Transcript expression of mitochondrial proteins on samples from TMCM, PPARα −/−, TMPD, and TMPDPA hearts. (d) Protein expression of mitochondrial proteins on samples from TMCM, PPARα −/−, TMPD, and TMPDPA hearts. (e) Transcript expression of mitochondrial fission and fusion proteins on samples from TMCM, PPARα −/|−, TMPD, and TMPDPA hearts. (f) Protein expression of mitochondrial fission and fusion proteins on samples from TMCM, PPARα −/−, TMPD, and TMPDPA hearts. (g) The mitochondrial DNA copy number on samples from TMCM, PPARα −/−, TMPD, and TMPDPA hearts. versus TMCM; versus TMCM.
