Differences in cardiac calcium release channel (ryanodine receptor) expression in myocardium from patients with end-stage heart failure caused by ischemic versus dilated cardiomyopathy [published erratum appears in Circ Res 1992 Dec;71(6):1538]

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Circulation Research. 1992;71:18-26

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Differences in cardiac calcium release channel (ryanodine receptor) expression in myocardium from patients with end-stage heart failure caused by ischemic versus dilated cardiomyopathy [published erratum appears in Circ Res 1992 Dec;71(6):1538]

AM Brillantes, P Allen, T Takahashi, S Izumo and AR Marks
Brookdale Center for Molecular Biology, Mount Sinai School of Medicine, New York, NY 10029.

The molecular basis for the systolic and diastolic dysfunction characteristic of end-stage heart failure in humans remains poorly understood. It has been proposed that both abnormal calcium handling and defects in the contractile apparatus may contribute to the myocardial dysfunction. Two channels, the calcium release channel (CRC) or ryanodine receptor of the sarcoplasmic reticulum (SR), and the slow calcium channel or dihydropyridine receptor (DHPR) of the transverse tubule, play key roles in regulating intracellular calcium concentration and in excitation-contraction (E-C) coupling in the heart. The DHPR serves as the voltage sensor and plasma membrane calcium channel resulting in activation of the CRC during E-C coupling in heart muscle. In this study, we investigated the levels of CRC expression in several forms of end-stage heart failure in humans. A cardiac CRC cDNA was cloned from rabbit and used as a probe for Northern blot analyses to determine mRNA levels in the left ventricles of normal (n = 4) and cardiomyopathic (n = 34) human hearts from patients undergoing cardiac transplantation. Compared with normal patients, patients with ischemic cardiomyopathy (n = 18) showed a 28% decrease in CRC mRNA levels (p less than 0.025) and patients with idiopathic dilated cardiomyopathy (n = 14) a nonsignificant 12% increase. In these same hearts, alpha-actin levels were unchanged in end-stage heart failure, as has been previously reported. This is the first report indicating that the expression of the CRC mRNA is abnormal in end-stage human heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

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				M. Anger, A.-M. Lompre, O. Vallot, F. Marotte, L. Rappaport, and J.-L. S. MD Cellular Distribution of Ca2+ Pumps and Ca2+ Release Channels in Rat Cardiac Hypertrophy Induced by Aortic Stenosis Circulation, December 1, 1998; 98(22): 2477 - 2486. [Abstract] [Full Text] [PDF]

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				G. Hasenfuss Alterations of calcium-regulatory proteins in heart failure Cardiovasc Res, February 1, 1998; 37(2): 279 - 289. [Full Text] [PDF]

				C.W. Balke and S. R. Shorofsky Alterations in calcium handling in cardiac hypertrophy and heart failure Cardiovasc Res, February 1, 1998; 37(2): 290 - 299. [Abstract] [Full Text] [PDF]

				R. M Phillips, P. Narayan, A. M Gomez, K. Dilly, L. R Jones, W.J. Lederer, and R. A Altschuld Sarcoplasmic reticulum in heart failure: central player or bystander? Cardiovasc Res, February 1, 1998; 37(2): 346 - 351. [Full Text] [PDF]

				M. Meyer and W. H Dillmann Sarcoplasmic reticulum Ca2+-ATPase overexpression by adenovirus mediated gene transfer and in transgenic mice Cardiovasc Res, February 1, 1998; 37(2): 360 - 366. [Abstract] [Full Text] [PDF]

				P. P de Tombe Altered contractile function in heart failure Cardiovasc Res, February 1, 1998; 37(2): 367 - 380. [Abstract] [Full Text] [PDF]

				K. R Sipido, T. Stankovicova, W. Flameng, J. Vanhaecke, and F. Verdonck Frequency dependence of Ca2+ release from the sarcoplasmic reticulum in human ventricular myocytes from end-stage heart failure Cardiovasc Res, February 1, 1998; 37(2): 478 - 488. [Abstract] [Full Text] [PDF]

				G.A. Ng, S. M Cobbe, and G. L Smith Non-uniform prolongation of intracellular Ca2+ transients recorded from the epicardial surface of isolated hearts from rabbits with heart failure Cardiovasc Res, February 1, 1998; 37(2): 489 - 502. [Abstract] [Full Text] [PDF]

				K. Mubagwa, P. Kaplan, B. Shivalkar, M. Miserez, V. Leunens, M. Borgers, and W. Flameng Calcium uptake by the sarcoplasmic reticulum, high energy content and histological changes in ischemic cardiomyopathy Cardiovasc Res, February 1, 1998; 37(2): 515 - 523. [Abstract] [Full Text] [PDF]

				R. Brauner, M. Nonoyama, H. Laks, D. C. Drinkwater Jr., S. McCaffery, T. Drake, A. J. Berk, L. Sen, and L. Wu INTRACORONARY ADENOVIRUS-MEDIATED TRANSFER OF IMMUNOSUPPRESSIVE CYTOKINE GENES PROLONGS ALLOGRAFT SURVIVAL J. Thorac. Cardiovasc. Surg., December 1, 1997; 114(6): 923 - 933. [Abstract] [Full Text]

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				R. Zucchi and S. Ronca-Testoni The Sarcoplasmic Reticulum Ca2+ Channel/Ryanodine Receptor: Modulation by Endogenous Effectors, Drugs and Disease States Pharmacol. Rev., March 1, 1997; 49(1): 1 - 52. [Abstract] [Full Text] [PDF]

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