Selective inhibition of HDAC2 by magnesium valproate attenuates cardiac hypertrophy

Canadian Journal of Physiology and Pharmacology

Volumn 95, Issue 3, 2016, Pages 260-267

  Raghunathan, Suchi ^a   Goyal, Ramesh K ^b   Patel, Bhoomika M ^a  

^a NIRMA UNIVERSITY   (India)

^b Delhi Institute of Pharmaceutical Sciences and Research   (India)

Author keywords

Class I HDAC; Class II HDAC; Magnesium valproate; Partial abdominal aortic constriction (PAAC)

Indexed keywords

C REACTIVE PROTEIN; CREATINE KINASE MB; GLUTATHIONE; HISTONE DEACETYLASE 2; HISTONE DEACETYLASE 5; LOW DENSITY LIPOPROTEIN; MALONALDEHYDE; MITOCHONDRIAL DNA; MYOCYTE ENHANCER FACTOR 2; SUPEROXIDE DISMUTASE; TRIACYLGLYCEROL; VALPROATE MAGNESIUM; VERY LOW DENSITY LIPOPROTEIN; BIOLOGICAL MARKER; HDAC2 PROTEIN, RAT; HDAC5 PROTEIN, RAT; HISTONE DEACETYLASE; HISTONE DEACETYLASE INHIBITOR; LIPID; VALPROIC ACID;

ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CHOLESTEROL BLOOD LEVEL; CONTROLLED STUDY; DRUG POTENCY; DYSLIPIDEMIA; ENZYME INHIBITION; GENE EXPRESSION; HEART RATE; HEART VENTRICLE HYPERTROPHY; HEART VENTRICLE PERFORMANCE; LIPOPROTEIN BLOOD LEVEL; MEAN ARTERIAL PRESSURE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; RAT; RISK ASSESSMENT; SURVIVAL RATE; TRIACYLGLYCEROL BLOOD LEVEL; ANIMAL; ANTAGONISTS AND INHIBITORS; BLOOD; CARDIAC MUSCLE; CARDIOMEGALY; DISEASE MODEL; DOWN REGULATION; DRUG EFFECTS; ENZYMOLOGY; FEMALE; GENE EXPRESSION REGULATION; GENETICS; HEART VENTRICLE REMODELING; HEMODYNAMICS; MALE; METABOLISM; PATHOLOGY; PATHOPHYSIOLOGY; TIME FACTOR; WISTAR RAT;

ANIMALS; BIOMARKERS; CARDIOMEGALY; DISEASE MODELS, ANIMAL; DNA, MITOCHONDRIAL; DOWN-REGULATION; FEMALE; GENE EXPRESSION REGULATION, ENZYMOLOGIC; HEMODYNAMICS; HISTONE DEACETYLASE 2; HISTONE DEACETYLASE INHIBITORS; HISTONE DEACETYLASES; LIPIDS; MALE; MYOCARDIUM; OXIDATIVE STRESS; RATS, WISTAR; TIME FACTORS; VALPROIC ACID; VENTRICULAR REMODELING;

EID: 85014709205     PISSN: 00084212     EISSN: 12057541     Source Type: Journal    
DOI: 10.1139/cjpp-2016-0542     Document Type: Article

References (45)

1. Ago, T., Kuroda, J., Pain, J., Fu, C., Li, H., and Sadoshima, J. 2010. Upregulation of Nox4 by hypertrophic stimuli promotes apoptosis and mitochondrial dysfunction in cardiac myocytes. Circ. Res. 106: 1253–1264. doi:10.1161/CIRCRESAHA. 109.213116.PMID20185797.
2. Anan, R., Nakagawa, M., Miyata, M., Higuchi, I., Nakao, S., Suehara, M., et al. 1995. Cardiac involvement in mitochondrial diseases: a study on 17 patients with documented mitochondrial DNA defects. Circulation, 91: 955–961. doi: 10.1161/01.CIR.91.4.955.PMID7850981.
3. Ay, H., Arsava, E.M., and Sarıbas, O. 2002. Creatine kinase-MB elevation after stroke is not cardiac in origin: comparison with troponin T levels. Stroke, 33: 286–289. doi:10.1161/hs0102.101544.PMID11779925.
4. Barja, G., and Herrero, A. 2000. Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heat and brain of mammals. FASEB J. 14: 312–318.PMID10657987.
5. Beutler, E., Duron, O., and Kelly, B.M. 1963. Improved method for the determination of blood glutathione. J. Lab. Clin. Med. 61: 882–888.PMID13967893.
6. Bradner, J.E., West, N., Grachan, M.L., Greenberg, E.F., Haggarty, S.J., Warnow, T., and Mazitschek, R. 2010. Chemical phylogenetics of histone deacetylases. Nat. Chem. Biol. 6: 238–243. doi:10.1038/nchembio.313.PMID 20139990.
7. Bugger, H., and Abel, E.D. 2010. Mitochondria in the diabetic heart. Cardiovasc. Res. 88: 229–240. doi:10.1093/cvr/cvq239.PMID20639213.
8. Cardinale, J.P., Sriramula, S., Pariaut, R., Guggilam, A., Mariappan, N., Elks, C.M., and Francis, J. 2010. HDAC inhibition attenuates inflammatory, hypertrophic, and hypertensive responses in spontaneously hypertensive rats. Hypertension, 56: 437–444. doi:10.1161/HYPERTENSIONAHA.110.154567.PMID20679181.
9. Chang, S., McKinsey, T.A., Zhang, C.L., Richardson, J.A., Hill, J.A., and Olson, E.N. 2004. Histone deacetylases 5 and 9 govern responsiveness of the heart to a subset of stress signals and play redundant roles in heart development. Mol. Cell. Biol. 24: 8467–8476. doi:10.1128/MCB.24.19.8467-8476.2004.PMID15367668.
10. Chittur, S.V., Sangster-Guity, N., and McCormick, P.J. 2008. Histone deacetylase inhibitors: a new mode for inhibition of cholesterol metabolism. BMC Genomics, 9: 507. doi:10.1186/1471-2164-9-507.PMID18959802.
11. Daosukho, C., Chen, Y., Noel, T., Sompol, P., Nithipongvanitch, R., Velez, J.M., et al. 2007. Phenylbutyrate, a histone deacetylase inhibitor, protects against Adriamycin-induced cardiac injury. Free Radical Biol. Med. 42: 1818–1825. doi:10.1016/j.freeradbiomed.2007.03.007.
12. Davila-Roman, V.G., Vedala, G., Herrero, P., de las Fuentes, L., Rogers, J.G., Kelly, D.P., and Gropler, R.J. 2002. Altered myocardial fatty acid and glucose metabolism in idiopathic dilated cardiomyopathy. J. Am. Coll. Cardiol. 40: 271–277. doi:10.1016/S0735-1097(02)01967-8.PMID12106931.
13. de Ruijter, A.J.M., van Gennip, A.H., Caron, H.N., Kemp, S., and van Kuilenburg, A.B.P. 2003. Histone deacetylases (HDACs): characterization of the classical HDAC family. Biochem. J. 370: 737–749. doi:10.1042/bj20021321.PMID12429021.
14. Frey, N., Katus, H.A., Olson, E.N., and Hill, J.A. 2004. Hypertrophy of the heart: a new therapeutic target? Circulation, 109: 1580–1589. doi:10.1161/01.CIR. 0000120390.68287.BB.PMID15066961.
15. Goyal, B.R., and Mehta, A.A. 2012. Beneficial role of spironolactone, telmisartan and their combination on isoproterenol induced cardiac hypertrophy. Acta Cardiol. 67: 203–211.PMID22641978.
16. Goyal, B.R., and Mehta, A.A. 2013. Diabetic cardiomyopathy: pathophysiological mechanisms and cardiac dysfunction. Hum. Exp. Toxicol. 32: 571–590. doi: 10.1177/0960327112450885.PMID23174745.
17. Goyal, B.R., Mesariya, P., Goyal, R.K., and Mehta, A.A. 2008. Effect of telmisartan on cardiovascular complications associated with streptozotocin diabetic rats. Mol. Cell. Biochem. 314: 123–131. doi:10.1007/s11010-008-9772-y.PMID18425420.
18. Goyal, B.R., Solanki, N., Goyal, R.K., and Mehta, A.A. 2009. Investigation into the cardiac effects of spironolactone in the experimental model of type 1 diabetes. J. Cardiovasc. Pharmacol. 54: 502–509. doi:10.1097/FJC.0b013e3181be75cc.PMID 19738487.
19. Goyal, B.R., Parmar, K., Goyal, R.K., and Mehta, A.A. 2011a. Beneficial role of telmisartan on cardiovascular complications associated with STZ-induced type 2 diabetes in rats. Pharmacol. Rep. 63: 956–966. doi:10.1016/S1734- 1140(11)70611-9.PMID22001983.
20. Goyal, B.R., Bhadada, S.V., and Patel, M.M. 2011b. Comparative evaluation of spironolactone, atenolol, metoprolol, ramipril and perindopril on diabetes induced cardiovascular complications in type 1 diabetes in rats. Int. J. Diabetes Metab. 19: 11–18.
21. Gregoretti, I.V., Lee, Y.M., and Goodson, H.V. 2004. Molecular evolution of the histone deacetylase family: functional implications of phylogenetic analysis. J. Mol. Biol. 338: 17–31. doi:10.1016/j.jmb.2004.02.006.PMID15050820.
22. Han, J.J., Hao, J., Kim, C.H., Hong, J.S., Ahn, H.Y., and Lee, Y.S. 2009. Quercetin prevents cardiac hypertrophy induced by pressure overload in rats. J. Vet. Med. Sci. 71: 737–743. doi:10.1292/jvms.71.737.PMID19578281.
23. Ide, T., Tsutsui, H., Hayashidani, S., Kang, D., Suematsu, N., Nakamura, K., et al. 2001. Mitochondrial DNA damage and dysfunction associated with oxidative stress in failing hearts after myocardial infarction. Circ. Res. 88: 529–535. doi:10.1161/01.RES.88.5.529.PMID11249877.
24. Karamanlidis, G., Bautista-Hernandez, V., Fynn-Thompson, F., Del Nido, P., and Tian, R. 2011. Impaired mitochondrial biogenesis precedes heart failure in right ventricular hypertrophy in congenital heart disease. Circ.: Heart Failure, 4: 707–713. doi:10.1161/CIRCHEARTFAILURE.111.961474.PMID21840936.
25. Kee, H.J., and Kook, H. 2011. Roles and targets of class I and IIa histone deacetylases in cardiac hypertrophy. J. Biomed. Biotechnol. 2011: 928326.PMID 21151616.
26. Kee, H.J., Sohn, I.S., Nam, K.I., Park, J.E., Qian, Y.R., Yin, Z., et al. 2006. Inhibition of histone deacetylation blocks cardiac hypertrophy induced by angiotensin II infusion and aortic banding. Circulation, 113: 51–59.PMID16380549.
27. Kook, H., Lepore, J.J., Gitler, A.D., Lu, M.M., Wing-Man Yung, W., Mackay, J., et al. 2003. Cardiac hypertrophy and histone deacetylase-dependent transcriptional repression mediated by the atypical homeodomain protein Hop. J. Clin. Invest. 112: 863–871. doi:10.1172/JCI19137.PMID12975471.
28. Kuroda, J., Ago, T., Matsushima, S., Zhai, P., Schneider, M.D., and Sadoshima, J. 2010. NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart. Proc. Natl. Acad. Sci. U.S.A. 107: 15565–15570. doi:10.1073/pnas. 1002178107.PMID20713697.
29. Lagace, D.C., and Nachtigal, M.W. 2004. Inhibition of histone deacetylase activity by valproic acid blocks adipogenesis. J. Biol. Chem. 279: 18851–18860. doi:10.1074/jbc.M312795200.PMID14985358.
30. Lowry, O.H., Rosenbrough, N.J., Farr, A.L., and Randall, R.J. 1951. Protein measurement with folin phenol reagent. J. Biol. Chem. 193: 265–275.PMID 14907713.
31. Maehara, K., Uekawa, N., and Isobe, K. 2002. Effects of histone acetylation on transcriptional regulation of manganese superoxide dismutase gene. Biochem. Biophys. Res. Commun. 295: 187–192. doi:10.1016/S0006-291X(02)00646-0.PMID 12083788.
32. Misra, H.P., and Fridovich, I. 1972. The role of superoxide anion in the autoxidation of epinephrine and a simple assay for superoxide dismutase. J. Biol. Chem. 247: 3170–3175.PMID4623845.
33. Ohkawa, H., Ohishi, N., and Yagi, K. 1979. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal. Biochem. 95: 351–358. doi:10. 1016/0003-2697(79)90738-3.PMID36810.
34. Patel, B.M., and Bhadada, S.V. 2014. Type 2 diabetes-induced cardiovascular complications: comparative evaluation of spironolactone, atenolol, metoprolol, ramipril and perindopril. Clin. Exp. Hypertens. 36(5): 340–347. doi:10.3109/ 10641963.2013.827699.PMID24047125.
35. Patel, B.M., and Desai, V.J. 2014. Beneficial role of tamoxifen in experimentally induced cardiac hypertrophy. Pharmacol. Rep. 66(2): 264–272. doi:10.1016/j. pharep.2014.02.004.PMID24911080.
36. Patel, B.M., and Mehta, A.A. 2012. Aldosterone and angiotensin: Role in diabetes and cardiovascular diseases. Eur. J. Pharmacol. 697: 1–12. doi:10.1016/j.ejphar. 2012.09.034.PMID23041273.
37. Patel, B.M., and Mehta, A.A. 2013. Choice of anti-hypertensive agents in diabetes subjects. Diabetes Vasc. Dis. Res. 10: 385–396. doi:10.1177/1479164113485250.
38. Patel, B.M., Agarwal, S.S., and Bhadada, S.V. 2012. Perindopril protects against streptozotocin-induced hyperglycemic myocardial damage/alterations. Hum. Exp. Toxicol. 31: 1132–1143. doi:10.1177/0960327112446817.PMID22653691.
39. Patel, B.M., Kakadiya, J., Goyal, R.K., and Mehta, A.A. 2013. Effect of spironolactone on cardiovascular complications associated with type-2 diabetes in rats. Exp. Clin. Endocrinol. Diabetes, 121: 441–447. doi:10.1055/s-0033-1345168.
40. Patel, B.M., Raghunathan, S., and Porwal, U. 2014. Cardioprotective effects of magnesium valproate in type 2 diabetes mellitus. Eur. J. Pharmacol. 728: 128–134. doi:10.1016/j.ejphar.2014.01.063.PMID24530414.
41. Raghunathan, S., and Patel, B.M. 2013. Therapeutic implications of small interfering RNA in cardiovascular diseases. Fundam. Clin. Pharmacol. 27: 1–20. doi:10.1111/j.1472-8206.2012.01051.x.PMID22762243.
42. Raghunathan, S., Tank, P., Bhadada, S.V., and Patel, B.M. 2014. Evaluation of buspirone on streptozotocin induced type 1 diabetes and its associated complications. BioMed Res. Int. 2014: 948427. doi:10.1155/2014/948427.PMID 24563867.
43. Rayabarapu, N., and Patel, B.M. 2014. Beneficial role of tamoxifen in isoproterenolinduced myocardial infarction. Can. J. Physiol. Pharmacol. 92(10): 849–857. doi:10.1139/cjpp-2013-0348.PMID25243890.
44. Trivedi, C.M., Luo, Y., Yin, Z., Zhang, M., Zhu, W., Wang, T., et al. 2007. Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3β activity. Nat. Med. 13: 324–331. doi:10.1038/nm1552.PMID17322895.
45. Zhang, C.L., McKinsey, T.A., Chang, S., Antos, C.L., Hill, J.A., and Olson, E.N. 2002. Class II histone deacetylases act as signal-responsive repressors of cardiac hypertrophy. Cell, 110: 479–488. doi:10.1016/S0092-8674(02)00861-9.PMID 12202037.