Phosphorylation status of regulatory proteins and functional characteristics in myocardium of dilated cardiomyopathy of Syrian hamsters

Journal of Physiological Sciences

Volumn 58, Issue 1, 2008, Pages 15-20

  Ohnuki, Yoshiki ^a   Nishimura, Satoshi ^b   Sugiura, Seiryo ^c   Saeki, Yasutake ^a  

^a TSURUMI UNIVERSITY   (Japan)

^b UNIVERSITY OF TOKYO   (Japan)

^c UNIVERSITY OF TOKYO   (Japan)

Author keywords

ATPase activity; Dilated cardiomyopathy; Phosphorylation status; Tension cost; Tension development

Indexed keywords

ADENOSINE TRIPHOSPHATASE; ADENOSINE TRIPHOSPHATE; CALCIUM ION; MYOSIN BINDING PROTEIN C; MYOSIN LIGHT CHAIN 2; TROPONIN I; TROPONIN T;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CALCIUM SIGNALING; CONGESTIVE CARDIOMYOPATHY; CONTROLLED STUDY; ENZYME ACTIVITY; HEART FUNCTION; HEART MUSCLE; MALE; NONHUMAN; PATHOPHYSIOLOGY; PROTEIN PHOSPHORYLATION; REGULATORY MECHANISM; SYRIAN HAMSTER; SYSTOLE;

ADENOSINE TRIPHOSPHATASES; ANIMALS; CALCIUM; CARDIAC MYOSINS; CARDIOMYOPATHY, DILATED; CARRIER PROTEINS; CRICETINAE; DIASTOLE; ISOMETRIC CONTRACTION; MALE; MESOCRICETUS; MUSCLE PROTEINS; MYOCARDIAL CONTRACTION; MYOCARDIUM; MYOSIN LIGHT CHAINS; PHOSPHORYLATION; SYSTOLE; TROPONIN I; TROPONIN T;

EID: 40049112958     PISSN: 18806546     EISSN: None     Source Type: Journal    
DOI: 10.2170/physiolsci.RP012807     Document Type: Article

References (36)

1. Dec GW, Fuster V. Idiopathic dilated cardiomyopathy. N Engl J Med. 1994;331:1564-75.
2. Panchal BC, Trippodo NC. Systemic and regional haemodynamics in conscious BIO T0-2 cardiomyopathic hamsters. Cardiovasc Res. 1993;27:2264-9.
3. Witte K, Schnecko A, Hauth D, Wirzius S, Lemmer B. Effects of chronic application of propranolol on β-adrenergic signal transduction in heart ventricles from myopathic BIO TO2 and control hamsters. Br J Pharmacol. 1998;125:1033-41.
4. Goineau S, Pape D, Guillo P, Ramee MP, Bellissant E. Hemodynamic and histomorphometric characteristics of dilated cardiomyopathy of Syrian hamsters (Bio TO-2 strain). Can J Physiol Pharmacol. 2001;79:329-37.
5. Iwase M, Kanazawa H, Kato Y, Nishizawa T, Somura F, Ishiki R, Nagata K, Hashimoto K, Takagi K, Izawa H, Yokota M. Growth hormone-releasing peptide can improve left ventricular dysfunction and attenuate dilation in dilated cardiomyopathic hamsters. Cardiovasc Res. 2004;61:30-8.
6. Nishizawa T, Iwase M, Kanazawa H, Ichihara S, Ichihara G, Nagata K, Obata K, Kitaichi K, Yokoi T, Watanabe M, Tsunematsu T, Ishikawa Y, Murohara T, Yokota M. Serial alterations of β-adrenergic signaling in dilated cardiomyopathic hamsters: possible role of myocardial oxidative stress. Circ J. 2004;68:1051-60.
7. Nishimura S, Yamashita H, Katoh M, Yamada KP, Sunagawa K, Saeki Y, Ohnuki Y, Nagai R, Sugiura S. Contractile dysfunction of cardiomyopathic hamster myocytes is pronounced under high load conditions. J Mol Cell Cardiol. 2005;39:231-9.
8. Sakamoto A, Ono K, Abe M, Jasmin G, Eki T, Murakami Y, Masaki T, Toyo-oka T, Hanaoka F. Both hypertrophic and dilated cardiomyopathies are caused by mutation of the same gene, δ-sarcoglycan, in hamster: an animal model of disrupted dystrophin-associated glycoprotein complex. Proc Natl Acad Sci USA. 1997;94:13873-8.
9. Sakamoto A, Abe M, Masaki T. Delineation of genomic deletion in cardiomyopathic hamster. FEBS Lett. 1999;447:124-8.
10. Tsubata S, Bowles KR, Vatta M, Zintz C, Titus J, Muhonen L, Bowles NE, Towbin JA. Mutations in the human δ-sarcoglycan gene in familial and sporadic dilated cardiomyopathy. J Clin Invest. 2000;106:655-62.
11. Malhotra A, Karell M, Scheuer J. Multiple cardiac contractile protein abnormalities in myopathic Syrian hamsters (BIO 53 : 58). J Mol Cell Cardiol. 1985;17:95-107.
12. Whitmer JT, Kumar P, Solaro RJ. Calcium transport properties of cardiac sarcoplasmic reticulum from cardiomyopathic Syrian hamsters (BIO 53.58 and 14.6): evidence for a quantitative defect in dilated myopathic hearts not evident in hypertrophic hearts. Circ Res. 1988;62:81-5.
13. 2+ pumps in heart and diaphragm of cardiomyopathic hamster: effects of perindopril. Am J Physiol. 1995;268:H1947-53.
14. Saeki Y, Kobayashi T, Minamisawa S, Sugi H. Protein kinase A increases the tension cost and unloaded shortening velocity in skinned rat cardiac muscle. J Mol Cell Cardiol. 1997;29:1655-63.
15. 2+-regulatory site of bovine cardiac troponin. J Biol Chem. 1982;257:260-3.
16. Hofmann PA, Lange JH 3rd. Effects of phosphorylation of troponin I and C protein on isometric tension and velocity of unloaded shortening in skinned single cardiac myocytes from rats. Circ Res. 1994;74:718-26.
17. 2+-stimulated MgATPase of reconstituted actomyosin S-1. J Biol Chem. 1995;270:25445-54.
18. Wolff MR, Buck SH, Stoker SW, Greaser ML, Mentzer RM. Myofibrillar calcium sensitivity of isometric tension is increased in human dilated cardiomyopathies: role of altered β-adrenergically mediated protein phosphorylation. J Clin Invest. 1996;98:167-76.
19. Messer AE, Jacques AM, Marston SB. Troponin phosphorylation and regulatory function in human heart muscle: dephosphorylation of Ser23/24 on troponin I could account for the contractile defect in end-stage heart failure. J Mol Cell Cardiol. 2007;42:247-59.
20. Morano I, Arndt H, Bachle-Stolz C, Ruegg JC. Further studies on the effects of myosin P-light chain phosphorylation on contractile properties of skinned cardiac fibres. Basic Res Cardiol. 1986;81:611-9.
21. 2+- stimulated actomyosin MgATPase activity. Biochem Biophys Res Commun. 1993;193:254-60.
22. 2+-sensitivity of force is enhanced in failing human hearts. Cardiovasc Res. 2003;57:505-14.
23. 2+- sensitivity of the contractile apparatus in end-stage human heart failure results from altered phosphorylation of contractile proteins. Cardiovasc Res. 2003;57:37-47.
24. Neumann J, Eschenhagen T, Jones LR, Linck B, Schmitz W, Scholz H, Zimmermann N. Increased expression of cardiac phosphatases in patients with end-stage heart failure. J Mol Cell Cardiol. 1997;29:265-72.
25. Carr AN, Schmidt AG, Suzuki Y, del Monte F, Sato Y, Lanner C, Breeden K, Jing SL, Allen PB, Greengard P, Yatani A, Hoit BD, Grupp IL, Hajjar RJ, DePaoli-Roach AA, Kranias EG. Type 1 phosphatase, a negative regulator of cardiac function. Mol Cell Biol. 2002;22:4124-35.
26. El-Armouche A, Pamminger T, Ditz D, Zolk O, Eschenhagen T. Decreased protein and phosphorylation level of the protein phosphatase inhibitor-1 in failing human hearts. Cardiovasc Res. 2004;61:87-93.
27. Bristow MR, Ginsburg R, Minobe W, Cubicciotti RS, Sageman WS, Lurie K, Billingham ME, Harrison DC, Stinson EB. Decreased catecholamine sensitivity and β-adrenergic-receptor density in failing human hearts. N Engl J Med. 1982;307:205-11.
28. Bristow MR, Minobe W, Rasmussen R, Larrabee P, Skerl L, Klein JW, Anderson FL, Murray J, Mestroni L, Karwande SV, Fowler M, Ginsburg R. β-adrenergic neuroeffector abnormalities in the failing human heart are produced by local rather than systemic mechanisms. J Clin Invest. 1992;89:803-15.
29. 1 receptor messenger RNA abundance in the failing human heart. J Clin Invest. 1993;92:2737-45.
30. Movsesian MA. Altered cAMP-mediated signalling and its role in the pathogenesis of dilated cardiomyopathy. Cardiovasc Res. 2004;62:450-9.
31. Feldman AM, Tena RG, Kessler PD, Weisman HF, Schulman SP, Blumenthal RS, Jackson DG, Van Dop C. Diminished β-adrenergic receptor responsiveness and cardiac dilation in hearts of myopathic Syrian hamsters (BIO 53.58) are associated with a functional abnormality of the G stimulatory protein. Circulation. 1990;81:1341-52.
32. 2+ on cross-bridge turnover kinetics in skinned single rabbit psoas fibers: implications for regulation of muscle contraction. Proc Natl Acad Sci USA. 1988;85:3265-9.
33. Kentish JC, McCloskey DT, Layland J, Palmer S, Leiden JM, Martin AF, Solaro RJ. Phosphorylation of troponin I by protein kinase A accelerates relaxation and crossbridge cycle kinetics in mouse ventricular muscle. Circ Res 2001;88:1059-65.
34. Stelzer JE, Patel JR, Moss RL. Acceleration of stretch activation in murine myocardium due to phosphorylation of myosin regulatory light chain. J Gen Physiol. 2006;128:261-72.
35. Layland J, Solaro RJ, Shah AM. Regulation of cardiac contractile function by troponin I phosphorylation. Cardiovasc Res. 2005;66:12-21.
36. Stelzer JE, Patel JR, Walker JW, Moss RL. Differential roles of cardiac myosinbinding protein C and cardiac troponin I in the myofibrillar force responses to protein kinase A phosphorylation. Circ Res. 2007;101:503-11.