Journal of Cardiac Failure
Volume 12, Issue 6 , Pages 479-486 , August 2006

P38 MAP Kinase Activity Is Correlated With Angiotensin II Type 1 Receptor Blocker–Induced Left Ventricular Reverse Remodeling in Spontaneously Hypertensive Heart Failure Rats

  • Qiangrong Liang, MD, PhD
    • ,
  • Andrew C. Elson, BS
    • ,
  • A. Martin Gerdes, PhD

      Affiliations

    • Corresponding Author InformationReprint requests: A. Martin Gerdes, PhD, Cardiovascular Research Institute, South Dakota Health Research Foundation, 1100 East 21st Street, Sioux Falls, SD 57105.

Received 16 December 2005 ,Revised 22 March 2006 ,Accepted 27 April 2006.

References 

  1. American Heart Association. Heart disease and stroke statistics—2006 update. Dallas (Tx): American Heart Association.
  2. Molkentin JD, Dorn IG. Cytoplasmic signaling pathways that regulate cardiac hypertrophy. Annu Rev Physiol. 2001;63:391–426
  3. Frey N, Olson EN. Cardiac hypertrophy: the good, the bad, and the ugly. Annu Rev Physiol. 2003;65:45–79
  4. Bueno OF, De Windt LJ, Tymitz KM, et al. The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice. EMBO J. 2000;19:6341–6350
  5. Bueno OF, Molkentin JD. Involvement of extracellular signal-regulated kinases 1/2 in cardiac hypertrophy and cell death. Circ Res. 2002;91:776–781
  6. Braz JC, Bueno OF, Liang Q, et al. Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling. J Clin Invest. 2003;111:1475–1486
  7. Liang Q, Bueno OF, Wilkins BJ, et al. c-Jun N-terminal kinases (JNK) antagonize cardiac growth through cross-talk with calcineurin-NFAT signaling. EMBO J. 2003;22:5079–5089
  8. Liang Q, Molkentin JD. Redefining the roles of p38 and JNK signaling in cardiac hypertrophy: dichotomy between cultured myocytes and animal models. J Mol Cell Cardiol. 2003;35:1385–1394
  9. McCune SAPS, Radin MJ, Jenkins JE, Chu YY, Park S. SHHF/MCC-fa cp. rat model: a genetic model of congestive heart failure. In:  Singal PK,  Dixon IMC,  Beamish RE,  Dhalla NS editor. Mechanisms of heart failure. Boston: Kluwer Academic Publishers; 1995;p. 91–106
  10. Anderson KM, Eckhart AD, Willette RN, et al. The myocardial beta-adrenergic system in spontaneously hypertensive heart failure (SHHF) rats. Hypertension. 1999;33:402–407
  11. Heyen JR, Blasi ER, Nikula K, et al. Structural, functional, and molecular characterization of the SHHF model of heart failure. Am J Physiol Heart Circ Physiol. 2002;283:H1775–H1784
  12. Bergman MR, Kao RH, McCune SA, et al. Myocardial tumor necrosis factor-alpha secretion in hypertensive and heart failure-prone rats. Am J Physiol. 1999;277:H543–H550
  13. Fowler MB, Vera-Llonch M, Oster G, et al. Influence of carvedilol on hospitalizations in heart failure: incidence, resource utilization and costs. US Carvedilol Heart Failure Study Group. J Am Coll Cardiol. 2001;37:1692–1699
  14. Kacimi R, Gerdes AM. Alterations in G protein and MAP kinase signaling pathways during cardiac remodeling in hypertension and heart failure. Hypertension. 2003;41:968–977
  15. Tamura T, Said S, Harris J, et al. Reverse remodeling of cardiac myocyte hypertrophy in hypertension and failure by targeting of the renin-angiotensin system. Circulation. 2000;102:253–259
  16. Tamura T, Said S, Andersen SM, et al. Temporal regression of myocyte hypertrophy in hypertensive, heart failure-prone rats treated with an AT1-receptor antagonist. J Card Fail. 2002;8:43–47
  17. Johnsen DD, Kacimi R, Anderson BE, et al. Protein kinase C isozymes in hypertension and hypertrophy: insight from SHHF rat hearts. Mol Cell Biochem. 2005;270:63–69
  18. Liang Q, De Windt LJ, Witt SA, et al. The transcription factors GATA4 and GATA6 regulate cardiomyocyte hypertrophy in vitro and in vivo. J Biol Chem. 2001;276:30245–30253
  19. Onodera T, Tamura T, Said S, et al. Maladaptive remodeling of cardiac myocyte shape begins long before failure in hypertension. Hypertension. 1998;32:753–757
  20. Wang Y, Huang S, Sah VP, et al. Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family. J Biol Chem. 1998;273:2161–2168
  21. Haq S, Choukroun G, Lim H, et al. Differential activation of signal transduction pathways in human hearts with hypertrophy versus advanced heart failure. Circulation. 2001;103:670–677
  22. Baba HA, Stypmann J, Grabellus F, et al. Dynamic regulation of MEK/Erks and Akt/GSK-3beta in human end-stage heart failure after left ventricular mechanical support: myocardial mechanotransduction-sensitivity as a possible molecular mechanism. Cardiovasc Res. 2003;59:390–399
  23. Communal C, Colucci WS, Remondino A, et al. Reciprocal modulation of mitogen-activated protein kinases and mitogen-activated protein kinase phosphatase 1 and 2 in failing human myocardium. J Card Fail. 2002;8:86–92
  24. Flesch M, Margulies KB, Mochmann HC, et al. Differential regulation of mitogen-activated protein kinases in the failing human heart in response to mechanical unloading. Circulation. 2001;104:2273–2276
  25. Hayashida W, Kihara Y, Yasaka A, et al. Stage-specific differential activation of mitogen-activated protein kinases in hypertrophied and failing rat hearts. J Mol Cell Cardiol. 2001;33:733–744
  26. Tamura T, Onodera T, Said S, et al. Correlation of myocyte lengthening to chamber dilation in the spontaneously hypertensive heart failure (SHHF) rat. J Mol Cell Cardiol. 1998;30:2175–2181
  27. Li M, Georgakopoulos D, Lu G, et al. p38 MAP kinase mediates inflammatory cytokine induction in cardiomyocytes and extracellular matrix remodeling in heart. Circulation. 2005;111:2494–2502
  28. Kaiser RA, Bueno OF, Lips DJ, et al. Targeted inhibition of p38 mitogen-activated protein kinase antagonizes cardiac injury and cell death following ischemia-reperfusion in vivo. J Biol Chem. 2004;279:15524–15530
  29. Kaiser RA, Lyons JM, Duffy JY, et al. Inhibition of p38 reduces myocardial infarction injury in the mouse but not pig after ischemia-reperfusion. Am J Physiol Heart Circ Physiol. Dec 2005;289:H2747–H2751
  30. Liu YH, Wang D, Rhaleb NE, et al. Inhibition of p38 mitogen-activated protein kinase protects the heart against cardiac remodeling in mice with heart failure resulting from myocardial infarction. J Card Fail. 2005;11:74–81
  31. Ma XL, Kumar S, Gao F, et al. Inhibition of p38 mitogen-activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion. Circulation. 1999;99:1685–1691
  32. Olzinski AR, McCafferty TA, Zhao SQ, et al. Hypertensive target organ damage is attenuated by a p38 MAPK inhibitor: role of systemic blood pressure and endothelial protection. Cardiovasc Res. 2005;66:170–178
  33. Petrich BG, Wang Y. Stress-activated MAP kinases in cardiac remodeling and heart failure; new insights from transgenic studies. Trends Cardiovasc Med. 2004;14:50–55
  34. Ren J, Zhang S, Kovacs A, et al. Role of p38alpha MAPK in cardiac apoptosis and remodeling after myocardial infarction. J Mol Cell Cardiol. 2005;38:617–623
  35. See F, Thomas W, Way K, et al. p38 mitogen-activated protein kinase inhibition improves cardiac function and attenuates left ventricular remodeling following myocardial infarction in the rat. J Am Coll Cardiol. 2004;44:1679–1689
  36. Liao P, Georgakopoulos D, Kovacs A, et al. The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy. Proc Natl Acad Sci U S A. 2001;98:12283–12288
  37. Martindale JJ, Wall JA, Martinez-Longoria DM, et al. Overexpression of mitogen-activated protein kinase kinase 6 in the heart improves functional recovery from ischemia in vitro and protects against myocardial infarction in vivo. J Biol Chem. 2005;280:669–676
  38. Nishida K, Yamaguchi O, Hirotani S, et al. p38alpha mitogen-activated protein kinase plays a critical role in cardiomyocyte survival but not in cardiac hypertrophic growth in response to pressure overload. Mol Cell Biol. 2004;24:10611–10620
  39. Ballard-Croft C, Kristo G, Yoshimura Y, et al. Acute adenosine preconditioning is mediated by p38 MAPK activation in discrete subcellular compartments. Am J Physiol Heart Circ Physiol. 2005;288:H1359–H1366
  40. Hoover HE, Thuerauf DJ, Martindale JJ, et al. alpha B-crystallin gene induction and phosphorylation by MKK6-activated p38. A potential role for alpha B-crystallin as a target of the p38 branch of the cardiac stress response. J Biol Chem. 2000;275:23825–23833

 Supported by grants HL-62459 and P20 RR017662 from the National Institutes of Health, and the South Dakota 2010 Program. The South Dakota Health Research Foundation is a partnership between the Sanford School of Medicine at the University of South Dakota and Sioux Valley Hospital and Health Systems in Sioux Falls. QL is supported by an American Heart Association Scientist Development Grant.

PII: S1071-9164(06)00226-0

doi: 10.1016/j.cardfail.2006.04.006

Journal of Cardiac Failure
Volume 12, Issue 6 , Pages 479-486 , August 2006

Article Tools

* Image Usage & Resolution