Extracellular signal-regulated kinases 1/2 as regulators of cardiac hypertrophy

Frontiers in Pharmacology

Volumn 6, Issue JUL, 2015, Pages

  Mutlak, Michael ^a   Kehat, Izhak ^a,b  

^a TECHNION ISRAEL INSTITUTE OF TECHNOLOGY   (Israel)

^b RAMBAM MEDICAL CENTER   (Israel)

Author keywords

Cardiac hypertrophy; Extracellular signal regulated kinases; Mitogen activated protein kinase; Mouse models; Signaling

Indexed keywords

DUAL SPECIFICITY PHOSPHATASE; DUAL SPECIFICITY PHOSPHATASE 10; DUAL SPECIFICITY PHOSPHATASE 16; DUAL SPECIFICITY PHOSPHATASE 4; DUAL SPECIFICITY PHOSPHATASE 6; DUAL SPECIFICITY PHOSPHATASE 8; EPIDERMAL GROWTH FACTOR RECEPTOR 2; G PROTEIN COUPLED RECEPTOR; HISTONE DEACETYLASE 1; LEUKEMIA INHIBITORY FACTOR; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE 1; MITOGEN ACTIVATED PROTEIN KINASE 3; MITOGEN ACTIVATED PROTEIN KINASE INHIBITOR; MITOGEN ACTIVATED PROTEIN KINASE PHOSPHATASE 1; MYC PROTEIN; MYOSIN HEAVY CHAIN BETA; N(G) NITROARGININE METHYL ESTER; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR ALPHA; PHOSPHATASE; PHOSPHOPROTEIN PHOSPHATASE 2A; PROTEIN C FOS; PROTEIN P53; PROTEIN TYROSINE KINASE; STRESS ACTIVATED PROTEIN KINASE; TRANSCRIPTION FACTOR ELK 1; TRANSCRIPTION FACTOR ETS 1; TRANSCRIPTION FACTOR ETS 2; TRANSCRIPTION FACTOR GATA 4; UNCLASSIFIED DRUG; UNINDEXED DRUG;

BIOACCUMULATION; CELL GROWTH; CELL PROLIFERATION; CELL VIABILITY; ENZYME ACTIVATION; HEART FUNCTION; HEART MUSCLE CELL; HEART VENTRICLE HYPERTROPHY; HUMAN; NONHUMAN; PHYSIOLOGICAL PROCESS; PROTEIN DEPHOSPHORYLATION; PROTEIN EXPRESSION; PROTEIN FUNCTION; PROTEIN MOTIF; PROTEIN PHOSPHORYLATION; PROTEIN TARGETING; REGULATORY MECHANISM; REVIEW; SIGNAL TRANSDUCTION;

EID: 84940033492     PISSN: None     EISSN: 16639812     Source Type: Journal    
DOI: 10.3389/fphar.2015.00149     Document Type: Review

References (42)

1. Albeck, J. G., Mills, G. B., and Brugge, J. S. (2013). Frequency-modulated pulses of ERK activity transmit quantitative proliferation signals. Mol. Cell. 49, 249-261. doi: 10.1016/j.molcel.2012.11.002.
2. Babu, G. J., Lalli, M. J., Sussman, M. A., Sadoshima, J., and Periasamy, M. (2000). Phosphorylation of elk-1 by MEK/ERK pathway is necessary for c-fos gene activation during cardiac myocyte hypertrophy. J. Mol. Cell Cardiol. 32, 1447-1457. doi: 10.1006/jmcc.2000.1185.
3. Bueno, O. F., De Windt, L. J., Tymitz, K. M., Witt, S. A., Kimball, T. R., Klevitsky, R., et al. (2000). The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice. EMBO J. 19, 6341-6350. doi: 10.1093/emboj/19.23.6341.
4. Bueno, O. F., and Molkentin, J. D. (2002). Involvement of extracellular signal-regulated kinases 1/2 in cardiac hypertrophy and cell death. Circ. Res. 91, 776-781. doi: 10.1161/01.RES.0000038488.38975.1A.
5. Caunt, C. J., and Keyse, S. M. (2013). Dual-specificity MAP kinase phosphatases (MKPs): shaping the outcome of MAP kinase signalling. FEBS J. 280, 489-504. doi: 10.1111/j.1742-4658.2012.08716.x.
6. Chatterjee, S., Bavishi, C., Sardar, P., Agarwal, V., Krishnamoorthy, P., Grodzicki, T., et al. (2014). Meta-analysis of left ventricular hypertrophy and sustained arrhythmias. Am. J. Cardiol. 114, 1049-1052. doi: 10.1016/j.amjcard.2014.07.015.
7. Cohen-Saidon, C., Cohen, A. A., Sigal, A., Liron, Y., and Alon, U. (2009). Dynamics and variability of ERK2 response to EGF in individual living cells. Mol. Cell. 36, 885-893. doi: 10.1016/j.molcel.2009.11.025.
8. D'Uva, G., Aharonov, A., Lauriola, M., Kain, D., Yahalom-Ronen, Y., Carvalho, S., et al. (2015). ERBB2 triggers mammalian heart regeneration by promoting cardiomyocyte dedifferentiation and proliferation. Nat. Cell Biol. 17, 627-638. doi: 10.1038/ncb3149.
9. Dickinson, R. J., and Keyse, S. M. (2006). Diverse physiological functions for dual-specificity MAP kinase phosphatases. J. Cell Sci. 119, 4607-4615. doi: 10.1242/jcs.03266.
10. Duncia, J. V., Santella, J. B. III, Higley, C. A., Pitts, W. J., Wityak, J., Frietze, W. E., et al. (1998). MEK inhibitors: the chemistry and biological activity of U0126, its analogs, and cyclization products. Bioorg. Med. Chem. Lett. 8, 2839-2844. doi: 10.1016/S0960-894X(98)00522-8.
11. El Azzouzi, H., Leptidis, S., Bourajjaj, M., Van Bilsen, M., Da Costa Martins, P. A., and De Windt, L. J. (2012). MEK1 inhibits cardiac PPARalpha activity by direct interaction and prevents its nuclear localization. PLoS ONE 7:e36799. doi: 10.1371/journal.pone.0036799.
12. English, J. M., and Cobb, M. H. (2002). Pharmacological inhibitors of MAPK pathways. Trends Pharmacol. Sci. 23, 40-45. doi: 10.1016/S0165-6147(00)01865-4.
13. Ferguson, B. S., Harrison, B. C., Jeong, M. Y., Reid, B. G., Wempe, M. F., Wagner, F. F., et al. (2013). Signal-dependent repression of DUSP5 by class I HDACs controls nuclear ERK activity and cardiomyocyte hypertrophy. Proc. Natl. Acad. Sci. U.S.A. 110, 9806-9811. doi: 10.1073/pnas.1301509110.
14. Fjeld, C. C., Rice, A. E., Kim, Y., Gee, K. R., and Denu, J. M. (2000). Mechanistic basis for catalytic activation of mitogen-activated protein kinase phosphatase 3 by extracellular signal-regulated kinase. J. Biol. Chem. 275, 6749-6757. doi: 10.1074/jbc.275.10.6749.
15. Gaasch, W. H., Delorey, D. E., St John Sutton, M. G., and Zile, M. R. (2008). Patterns of structural and functional remodeling of the left ventricle in chronic heart failure. Am. J. Cardiol. 102, 459-462. doi: 10.1016/j.amjcard.2008.03.081.
16. Gaasch, W. H., and Zile, M. R. (2011). Left ventricular structural remodeling in health and disease: with special emphasis on volume, mass, and geometry. J. Am. Coll. Cardiol. 58, 1733-1740. doi: 10.1016/j.jacc.2011.07.022.
17. Goktepe, S., Abilez, O. J., Parker, K. K., and Kuhl, E. (2010). A multiscale model for eccentric and concentric cardiac growth through sarcomerogenesis. J. Theor. Biol. 265, 433-442. doi: 10.1016/j.jtbi.2010.04.023.
18. Grossman, W., and Paulus, W. J. (2013). Myocardial stress and hypertrophy: a complex interface between biophysics and cardiac remodeling. J. Clin. Invest. 123, 3701-3703. doi: 10.1172/JCI69830.
19. Kehat, I., Davis, J., Tiburcy, M., Accornero, F., Saba-El-Leil, M. K., Maillet, M., et al. (2011). Extracellular signal-regulated kinases 1 and 2 regulate the balance between eccentric and concentric cardiac growth. Circ. Res. 108, 176-183. doi: 10.1161/CIRCRESAHA.110.231514.
20. Kehat, I., and Molkentin, J. D. (2010a). Extracellular signal-regulated kinase 1/2 (ERK1/2) signaling in cardiac hypertrophy. Ann. N. Y. Acad. Sci. 1188, 96-102. doi: 10.1111/j.1749-6632.2009.05088.x.
21. Kehat, I., and Molkentin, J. D. (2010b). Molecular pathways underlying cardiac remodeling during pathophysiological stimulation. Circulation 122, 2727-2735. doi: 10.1161/CIRCULATIONAHA.110.942268.
22. Kodama, H., Fukuda, K., Pan, J., Sano, M., Takahashi, T., Kato, T., et al. (2000). Significance of ERK cascade compared with JAK/STAT and PI3-K pathway in gp130-mediated cardiac hypertrophy. Am. J. Physiol. Heart Circ. Physiol. 279, H1635-H1644.
23. La Gerche, A., and Prior, D. L. (2007). Exercise-is it possible to have too much of a good thing? Heart Lung. Circ. 16(Suppl. 3), S102-S104. doi: 10.1016/j.hlc.2007.03.014.
24. Li, H., He, C., Feng, J., Zhang, Y., Tang, Q., Bian, Z., et al. (2010). Regulator of G protein signaling 5 protects against cardiac hypertrophy and fibrosis during biomechanical stress of pressure overload. Proc. Natl. Acad. Sci. U.S.A. 107, 13818-13823. doi: 10.1073/pnas.1008397107.
25. Liang, F., Lu, S., and Gardner, D. G. (2000). Endothelin-dependent and-independent components of strain-activated brain natriuretic peptide gene transcription require extracellular signal regulated kinase and p38 mitogen-activated protein kinase. Hypertension 35, 188-192. doi: 10.1161/01.HYP.35.1.188.
26. Lips, D. J., Bueno, O. F., Wilkins, B. J., Purcell, N. H., Kaiser, R. A., Lorenz, J. N., et al. (2004). MEK1-ERK2 signaling pathway protects myocardium from ischemic injury in vivo. Circulation 109, 1938-1941. doi: 10.1161/01.CIR.0000127126.73759.23.
27. Lorenz, K., Schmitt, J. P., Schmitteckert, E. M., and Lohse, M. J. (2009). A new type of ERK1/2 autophosphorylation causes cardiac hypertrophy. Nat. Med. 15, 75-83. doi: 10.1038/nm.1893.
28. Maillet, M., Purcell, N. H., Sargent, M. A., York, A. J., Bueno, O. F., and Molkentin, J. D. (2008). DUSP6 (MKP3) null mice show enhanced ERK1/2 phosphorylation at baseline and increased myocyte proliferation in the heart affecting disease susceptibility. J. Biol. Chem. 283, 31246-31255. doi: 10.1074/jbc.M806085200.
29. Markou, T., Hadzopoulou-Cladaras, M., and Lazou, A. (2004). Phenylephrine induces activation of CREB in adult rat cardiac myocytes through MSK1 and PKA signaling pathways. J. Mol. Cell Cardiol. 37, 1001-1011. doi: 10.1016/j.yjmcc.2004.08.002.
30. Munzel, F., Muhlhauser, U., Zimmermann, W. H., Didie, M., Schneiderbanger, K., Schubert, P., et al. (2005). Endothelin-1 and isoprenaline co-stimulation causes contractile failure which is partially reversed by MEK inhibition. Cardiovasc. Res. 68, 464-474. doi: 10.1016/j.cardiores.2005.06.020.
31. Nayak, J., Gastonguay, A. J., Talipov, M. R., Vakeel, P., Span, E. A., Kalous, K. S., et al. (2014). Protein expression, characterization and activity comparisons of wild type and mutant DUSP5 proteins. BMC Biochem. 15:27. doi: 10.1186/s12858-014-0027-0.
32. Purcell, N. H., Wilkins, B. J., York, A., Saba-El-Leil, M. K., Meloche, S., Robbins, J., et al. (2007). Genetic inhibition of cardiac ERK1/2 promotes stress-induced apoptosis and heart failure but has no effect on hypertrophy in vivo. Proc. Natl. Acad. Sci. U.S.A. 104, 14074-14079. doi: 10.1073/pnas.0610906104.
33. Ruppert, C., Deiss, K., Herrmann, S., Vidal, M., Oezkur, M., Gorski, A., et al. (2013). Interference with ERK(Thr188) phosphorylation impairs pathological but not physiological cardiac hypertrophy. Proc. Natl. Acad. Sci. U.S.A. 110, 7440-7445. doi: 10.1073/pnas.1221999110.
34. 2+ blockers prevent myocardial remodeling induced by chronic NO inhibition in rats. Hypertension 41, 963-967. doi: 10.1161/01.HYP.0000062881.36813.7A.
35. Shaul, Y. D., and Seger, R. (2007). The MEK/ERK cascade: from signaling specificity to diverse functions. Biochim. Biophys. Acta 1773, 1213-1226. doi: 10.1016/j.bbamcr.2006.10.005.
36. Spinale, F. G. (2007). Myocardial matrix remodeling and the matrix metalloproteinases: influence on cardiac form and function. Physiol. Rev. 87, 1285-1342. doi: 10.1152/physrev.00012.2007.
37. Tenhunen, O., Sarman, B., Kerkela, R., Szokodi, I., Papp, L., Toth, M., et al. (2004). Mitogen-activated protein kinases p38 and ERK 1/2 mediate the wall stress-induced activation of GATA-4 binding in adult heart. J. Biol. Chem. 279, 24852-24860. doi: 10.1074/jbc.M314317200.
38. van Berlo, J. H., Elrod, J. W., Aronow, B. J., Pu, W. T., and Molkentin, J. D. (2011). Serine 105 phosphorylation of transcription factor GATA4 is necessary for stress-induced cardiac hypertrophy in vivo. Proc. Natl. Acad. Sci. U.S.A. 108, 12331-12336. doi: 10.1073/pnas.1104499108.
39. Weeks, K. L., and McMullen, J. R. (2011). The athlete's heart vs. the failing heart: can signaling explain the two distinct outcomes? Physiology 26, 97-105. doi: 10.1152/physiol.00043.2010.
40. Wellbrock, C., Karasarides, M., and Marais, R. (2004). The RAF proteins take centre stage. Nat. Rev. Mol. Cell Biol. 5, 875-885. doi: 10.1038/nrm1498.
41. Yue, T. L., Gu, J. L., Wang, C., Reith, A. D., Lee, J. C., Mirabile, R. C., et al. (2000). Extracellular signal-regulated kinase plays an essential role in hypertrophic agonists, endothelin-1 and phenylephrine-induced cardiomyocyte hypertrophy. J. Biol. Chem. 275, 37895-37901. doi: 10.1074/jbc.M007037200.
42. Zhong, W., Mao, S., Tobis, S., Angelis, E., Jordan, M. C., Roos, K. P., et al. (2006). Hypertrophic growth in cardiac myocytes is mediated by Myc through a Cyclin D2-dependent pathway. EMBO J. 25, 3869-3879. doi: 10.1038/sj.emboj.7601252.