Deactivation of peroxisome proliferator-activated receptor-α during cardiac hypertrophic growth

Journal of Clinical Investigation

Volumn 105, Issue 12, 2000, Pages 1723-1730

  Barger, Philip M ^a   Brandt, Jon M ^a   Leone, Teresa C ^a   Weinheimer, Carla J ^a   Kelly, Daniel P ^a  

^a WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CARNITINE PALMITOYLTRANSFERASE; PALMITIC ACID; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; ENERGY BALANCE; FATTY ACID TRANSPORT; GENE EXPRESSION; GENE REPRESSION; HEART VENTRICLE HYPERTROPHY; NONHUMAN; OXIDATION; PRIORITY JOURNAL; RAT;

EID: 0033933236     PISSN: 00219738     EISSN: None     Source Type: Journal    
DOI: 10.1172/JCI9056     Document Type: Article

References (37)

1. Bing, R.J. 1955. The metabolism of the heart. Harvey Lect. 50:27-70.
2. Bremer, J., and Osmundson, H. 1984. Fatty acid oxidation and its regulation. In Fatty acid metabolism and its regulation. S. Numa, editor. Elsevier Science. Amsterdam, The Netherlands. 113-154.
3. Wittels, B., and Bressler, R. 1965. Lipid metabolism in the newborn heart. J. Clin. Invest. 44:1639-1646.
4. Kelly, D.P., and Strauss, A.W. 1994. Inherited cardiomyopathies. N. Engl. J. Med. 330:913-919.
5. Gulick, T., Cresci, S., Caira, T., Moore, D.D., and Kelly, D.P. 1994. The peroxisome proliferator activated receptor regulates mitochondrial fatty acid oxidative enzyme gene expression. Proc. Natl. Acad. Sci. USA. 91:11012-11016.
6. Carter, M.E., Gulick, T., Moore, D.D., and Kelly, D.P. 1994. A pleiotropic element in the medium-chain acyl coenzyme A dehydrogenase gene promoter mediates transcriptional regulation by multiple nuclear receptor transcription factors and defines novel receptor-DNA binding motifs. Mol. Cell. Biol. 14:4360-4372.
7. Disch, D.L., et al. 1996. Transcriptional control of a nuclear gene encodings mitochondrial fatty acid oxidation enzyme in transgenic mice: role for nuclear receptors in cardiac and brown adipose expression. Mol. Cell. Biol. 16:4043-4051.
8. Issemann, I., and Green, S. 1990. Activation of a member of the steroid hormone receptor superfamily by peroxisome proliferators. Nature. 347:645-650.
9. Brandt, J., Djouadi, F., and Kelly, D.P. 1998. Fatty acids activate transcription of the muscle carnitine palmitoyltransferase I gene in cardiac myocytes via the peroxisome proliferator-activated receptor α. J. Biol. Chem. 273:23786-23793.
10. Mascaró, C., et al. 1998. Control of human muscle-type carnitine palmitoyltransferase I gene transcription by peroxisome proliferator-activated receptor. J. Biol. Chem. 273:8560-8563.
11. Forman, B.M., Chen, J., and Evans, R.M. 1997. Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors α and δ. Proc. Natl. Acad. Sci. USA. 94:4312-4317.
12. Lee, S.S.T., et al. 1995. Targeted disruption of the α isoform of the peroxisome proliferator-activated receptor gene in mice results in abolishment of the pleiotropic effects of peroxisome proliferators. Mol. Cell. Biol. 15:3012-3022.
13. Aoyama, T., et al. 1998. Altered constitutive expression of fatty acid-metabolizing enzymes in mice lacking the peroxisome proliferator-activated receptor α (PPARα). J. Biol. Chem. 273:5678-5684.
14. Djouadi, F., et al. 1998. A gender-related defect in lipid metabolism and glucose homeostasis in peroxisome proliferator-activated receptor α-deficient mice. J. Clin. Invest. 102:1083-1091.
15. Leone, T.C., Weinheimer, C.J., and Kelly, D.P. 1999. A critical role for the peroxisome proliferator-activated receptor alpha (PPARα) in the cellular fasting response: the PPARα-null mouse as a model of fatty acid oxidation disorders. Proc. Natl. Acad. Sci. USA. 96:7473-7478.
16. Bishop, S.P., and Altschuld, R.A. 1970. Increased glycolytic metabolism in cardiac hypertrophy and congestive failure. Am. J. Physiol. 218:153-159.
17. Taegtmeyer, H., and Overturf, M.L. 1988. Effects of moderate hypertension on cardiac function and metabolism in the rabbit. Hypertension. 11:416-426.
18. Christe, M.D., and Rodgers, R.L. 1994. Altered glucose and fatty acid oxidation in hearts of the spontaneously hypertensive rat. J. Mol. Cell. Cardiol. 26:1371-1375.
19. Sack, M.N., et al. 1996. Fatty acid oxidation enzyme is downregulated in the failing heart. Circulation. 94:2837-2842.
20. Sack, M.N., Disch, D.L., Rockman, H.A., and Kelly, D.P. 1997. A role for Sp and nuclear receptor transcription factors in a cardiac hypertrophic growth program. Proc. Natl. Acad. Sci. USA. 94:6438-6443.
21. Marcus, S.L., et al. 1993. Diverse peroxisome proliferator-activated receptors bind to the peroxisome proliferator-responsive elements of the rat hydratase/dehydrogenase and fatty acyl-CoA oxidase genes but differentially induce expression. Proc. Natl. Acad. Sci. USA. 90:5723-5727.
22. Vega, R., Huss, J.M., and Kelly, D.P. 2000. The coactivator PGC-1 cooperates with PPARα in transcriptional control of nuclear genes encoding mitochondrial fatty acid oxidation enzymes. Mol. Cell. Biol. 20:1868-1876.
23. Strauss, A.W., et al. 1995. Molecular basis of human mitochondrial very-long-chain acyl-CoA dehydrogenase deficiency causing cardiomyopathy and sudden death in childhood. Proc. Natl. Acad. Sci. USA. 92:10496-10500.
24. Rogers, J.H., et al. 1999. RGS4 causes increased mortality and reduced cardiac hypertrophy in response to pressure overload. J. Clin. Invest. 104:567-576.
25. McGarry, J.D., Woeltje, K.F., Kuwajima, M., and Foster, D.W. 1989. Regulation of ketogenesis and the renaissance of carnitine palmitoyltransferase. Diabetes Metab. Rev. 5:271-284.
26. Yu, G.S., Lu, Y.C., and Gulick, T. 1998. Co-regulation of tissue-specific alternative human carnitine palmitoyltransferase 1β gene promoters by fatty acid enzyme substrate. J. Biol. Chem. 273:32901-32909.
27. Sugden, P.H. 1999. Signaling in myocardial hypertrophy. Life after calcineurin? Circ. Res. 84:633-646.
28. Juge-Aubry, C.E., et al. 1999. Regulation of the transcriptional activity of the peroxisome proliferator-activared receptor α by phosphorylation of a ligand-independent trans-activating domain. J. Biol. Chem. 274:10505-10510.
29. Hu, E., Kim, J.B., Sarraf, P., and Spiegelman, B.M. 1996. Inhibition of adipogenesis through MAP kinase-mediated phosphorylation of PPARγ. Science. 274:2100-2103.
30. Thorburn, A., et al. 1993. HRas-dependent pathways can activate morphological and genetic markers of cardiac muscle cell hypertrophy. J. Biol. Chem. 268:2244-2249.
31. Thorburn, A. 1994. Ras activity is required for phenylephrine-induced activation of mitogen-activated protein kinase in cardiac muscle cells. Biochem. Biophys. Res. Commun. 205:1417-1422.
32. Gillespie-Brown, J., Fuller, S.J., Bogoyevitch, M.A., Cowley, S., and Sugden, P.H. 1995. The mitogen-activated protein kinase kinase MEK1 stimulates a pattern of gene expression typical of rhe hypertrophic phenotype in rat ventricular cardiomyocytes. J. Biol. Chem. 270:28092-28096.
33. Zechner, D., Thuerauf, D.J., Hanford, D.S., McDonough, P.M., and Glembotski, C.C. 1997. A role for the p38 mitogen-activated protein kinase pathway in myocardial cell growth, sarcomeric organization, and cardiac-specific gene expression. J. Cell Biol. 139:115-127.
34. 2-terminal kinases. J. Clin. Invest. 104:391-398.
35. Molkentin, J.D., et al. 1998. A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Cell. 93:215-228.
36. Corr, P.B., Creer, M.H., Yamada, K.A., Saffitz, J.E., and Sobel, B.E. 1989. Prophylaxis of early ventricular fibrillation by inhibition of acylcarnitine accumulation. J. Clin. Invest. 83:927-936.
37. Stanley, C.A., et al. 1992. A deficiency of carnitine-acylcarnitine translocase in the inner mitochondrial membrane. N. Engl. J. Med. 327:19-23.