Remodelling of ionic currents in hypertrophied and failing hearts of transgenic mice overexpressing calsequestrin

Journal of Physiology

Volumn 525, Issue 2, 2000, Pages 483-498

  Knollmann, Björn C ^a   Knollmann Ritschel, Barbara E C ^b   Weissman, Neil J ^c   Jones, Larry R ^d   Morad, Martin ^a  

^a GEORGETOWN UNIVERSITY MEDICAL CENTER   (United States)

^b WALTER REED ARMY MEDICAL CENTER   (United States)

^c WASHINGTON HOSPITAL CENTER   (United States)

^d INDIANA UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

8 BROMO CYCLIC AMP; CALCIUM ION; CALSEQUESTRIN; CYCLIC AMP; ISOBUTYLMETHYLXANTHINE; ISOPRENALINE; POTASSIUM ION; SODIUM ION;

AGE; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CALCIFICATION; CALCIUM CURRENT; CONTROLLED STUDY; FIBROSING ALVEOLITIS; HEART DILATATION; HEART FAILURE; HEART MUSCLE CELL; HEART VENTRICLE HYPERTROPHY; HUMAN; ION CURRENT; MOUSE; NERVE BLOCK; NEWBORN; NONHUMAN; POTASSIUM CURRENT; PR INTERVAL; PRIORITY JOURNAL; PROTEIN EXPRESSION; QT INTERVAL; SODIUM CURRENT; TRANSGENIC MOUSE; BETA ADRENERGIC STIMULATION; BLOOD VESSEL CAPACITANCE; HEART ATRIUM REMODELING; HEART CONDUCTION; HEART CONTRACTION; HEART ELECTROPHYSIOLOGY; HEART HYPERTROPHY; HEART MUSCLE FIBROSIS; HEART MUSCLE POTENTIAL; HISTOPATHOLOGY; INWARD RECTIFYING POTASSIUM CURRENT; PROTEIN ANALYSIS; QT PROLONGATION; SODIUM CALCIUM EXCHANGE; STEADY STATE; SURVIVAL RATE; TRANSIENT OUTWARD POTASSIUM CURRENT;

EID: 0034212795     PISSN: 00223751     EISSN: None     Source Type: Journal    
DOI: 10.1111/j.1469-7793.2000.t01-1-00483.x     Document Type: Article

References (38)

1. BARRY, D. M., XU, H., SCHUESSLER, R. B. & NERBONNE, J. M. (1998). Functional knockout of the transient outward current, long-QT syndrome and cardiac remodeling in mice ex pressing a dominant-negative Kv4 α subunit. Circulation Research 83, 560-567.
2. BERUL, C. I., CHRISTE, M. E., ARONOVITZ, M. J., SEIDMAN, C. E., SEIDMAN, J. G. & MENDELSOHN, M. E. (1997). Electrophysiological abnormalities and arrhythmias in α MHC mutant familial hypertrophic cardiomyopathy mice. Journal of Clinical Investigation 99, 570-576.
3. + currents in isolated human ventricular myocytes from patients with terminal heart failure. Circulation Research 73, 379-385.
4. CERBAI, E., BARBIERI, M., LI, Q. & MUGELLI, A. (1994). Ionic basis of action potential prolongation of hypertrophied cardiac myocytes isolated from hypertensive rats of different ages. Cardiovascular Research 28, 1180-1187.
5. CHO, M. C., RAPACCIUOLO, A., KOCH, W. J., KOBAYASHI, Y., JONES, L. R. & ROCKMAN, H. A. (1999). Defective β-adrenergic receptor signaling precedes the development of dilated cardiomyopathy in transgenic mice with calsequestrin overexpression. Journal of Biological Chemistry 274, 22251-22256.
6. 2+ transients and contraction. Journal of Physiology 432, 283-312.
7. COLBERT, M. C., HALL, D. G., KIMBALL, T. R., WITT, S. A., LORENZ, J. N., KIRBY, M. L., HEWETT, T. E., KLEVITSKY, R. & ROBBINS, J. (1997). Cardiac compartment-specific overexpression of a modified retinoic acid receptor produces dilated cardiomyopathy and congestive heart failure in transgenic mice. Journal of Clinical Investigation 100, 1958-1968.
8. D'ANGELO, D. D., SAKATA, Y., LORENZ, J. N., BOIVIN, G. P., WALSH, R. A., LIGGETT, S. B. & DORN, G. W. II (1997). Transgenic Gαq overexpression induces cardiac contractile failure in mice. Proceedings of the National Academy of Sciences of the USA 94, 8121-8126.
9. FENTZKE, R. C., KORCARZ, C. E., LANG, R. M., LIN, H. & LEIDEN, J. M. (1998). Dilated cardiomyopathy in transgenic mice expressing a dominant-negative CREB transcription factor in the heart. Journal of Clinical Inventigation 101, 2415-2426.
10. HASENFUSS, G., MEYER, M., SCHILLINGER, W., PREUSS, M., PIESKE, B. & JUST, H. (1997). Calcium handling proteins in the failing human heart. Basic Research in Cardiology 92 (suppl. 1), 87-93.
11. 2+ exchange activity in cardiomyopathic Syrian hamster. Circulation Research 74, 253-261.
12. 2+ signaling in transgenic mouse cardiac myocytes overexpressing calsequestrin. Journal of Clinical Investigation 101, 1385-1393.
13. KAAB, S., NUSS, H. B., CHIAMVIMONVAT, N., O'ROURKE, B., PAK, P. H., KASS, D. A., MARBAN, E. & TOMASELLI, G. F. (1996). Ionic mechanism of action potential prolongation in ventricular myocytes from dogs with pacing-induced heart failure. Circulation Research 78, 262-273.
14. KNOLLMANN, B. C., DUC, J., GROTH, A., WEISSMANN, N. J., CLEEMANN, L. & MORAD, M. (1998a). Cardiac phenotype of transgenic mice overexpressing calsequestrin (abstract). Circulation 98 (suppl. 1), I-1490.
15. KNOLLMANN, B. C., JONES, L. R. & MORAD, M. (1998b). Electrophysiological properties of transgenic myocytes overexpressing cardiac calsequestrin (abstract). Circulation 98 (suppl. 1), I-187.
16. + channel in human cardiac myocytes. Alterations in channel behavior in myocytes isolated from patients with idiopathic dilated cardiomyopathy. Circulation 92, 164-174.
17. KUBOTA, T., MCTIERNAN, C. F., FRYE, C. S., SLAWSON, S. E., LEMSTER, B. H., KORETSKY, A. P., DEMETRIS, A. .J. & FELDMAN, A. M. (1997). Dilated cardiomyopathy in transgenic mice with cardiac-specific overexpression of tumor necrosis factor-α. Circulation Research 81, 627-635.
18. LEBLANC, N., CHARTIER, D., GOSSELIN, H. & ROULEAU, J. L. (1998). Age and gender differences in excitation-contraction coupling of the rat ventricle. Journal of Physiology 511, 533-548.
19. LINCK, B., NEUMANN, J., HUKE, S., KIRCHHEFER, U., SCHMITZ, W., VOLKERY, F. & JONES, L. R. (1998). Functional alterations in mice overexpressing calsequestrin in the heart (abstract). Circulation 98 (suppl. 1), I-490.
20. 2+ exchange in the infarcted heart. Implications for excitation-contraction coupling. Circulation Research 81, 1083-1093.
21. LONDON, B., JERON, A., ZHOU, J., BUCKETT, P., HAN, X., MITCHELL, G. F. & KOREN, G. (1998a). Long QT and ventricular arrhythmias in transgenic mice expressing the N terminus and first transmembrane segment of a voltage-gated potassium channel. Proceedings of the National Academy of Sciences of the USA 95, 2926-2931.
22. LONDON, B., WANG, D. W., HILL, J. A. & BENNETT, P. B. (1998b). The transient outward current in mice lacking the potassium channel gene Kv1.4. Journal of Physiology 509, 171-182.
23. MENDE, U., KAGEN, A., COHEN, A., ARAMBURU, J., SCHOEN, F. J. & NEER, E. J. (1998). Transient cardiac expression of constitutively active Gαq leads to hypertrophy and dilated cardiomyopathy by calcineurin-dependent and independent pathways Proceedings of the National Academy of Sciences of the USA 95, 13893-13898.
24. MITCHELL, G. F., JERON, A. & KOREN, G. (1998). Measurement of heart rate and Q-T interval in the conscious mouse. American Journal of Physiology 274, H747-751.
25. MITRA, R. & MORAD, M. (1985). A uniform enzymatic method for dissociation of myocytes from hearts and stomachs of vertebrates. American Journal of Physiology 249, H1056-1060.
26. MOMTAZ, A., COULOMBE, A., RICHER, P., MERCADIER, J. J. & CORABOEUF, E. (1996). Action potential and plateau ionic currents in moderately and severely DOCA-salt hypertrophied rat hearts. Journal of Molecular and Cellular Cardiology 28, 2511-2522.
27. MURPHY, B. J., ROGERS, J., PERDICHIZZI, A. P., COLVIN, A. A. & CATTERALL, W. A. (1996). cAMP-dependent phosphorylation of two sites in the α subunit of the cardiac sodium channel. Journal of Biological Chemistry 271, 28837-28843.
28. NABAUER, M. & KAAB, S. (1998). Potassium channel downregulation in heart failure. Cardiovascular Research 37, 324-334.
29. O'ROURKE, B., KASS, D. A., TOMASELLI, G. F., KAAB, S., TUNIN, R. & MARBAN, E. (1999). Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, I: experimental studies. Circulation Research 84, 562-570.
30. PAN, X.-H., BAKER, L., LEE, J. S., KUBOTA, T., FELDMAN, A. M., SALAMA, G. & LONDON, B. (1998). Atrial and ventricular arrhythmias in transgenic mice with myocardial expression of TNF-α (abstract). Circulation 98 (suppl. 1), I-745.
31. RIGG, L. & TERRAR, D. A. (1996). Possible role of calcium release from the sarcoplasmic reticulum in pacemaking in guinea-pig sino-atrial node. Experimental Physiology 81, 877-880.
32. SATO, Y., FERGUSON, D. G., SAKO, H., DORN, G. W. II, KADAMBI, V.J., YATANI, A., HOIT, B. D., WALSH, R. A. & KRANIAS, E. G. (1998). Cardiac-specific overex pression of mouse cardiac calsequestrin is associated with depressed cardiovascular function and hypertrophy in transgenic mice. Journal of Biological Chemistry 273, 28470-28477.
33. SCOTT, B. T., SIMMERMAN, H. K., COLLINS, J. H., NADAL-GINARD, B. & JONES, L. R. (1988). Complete amino acid sequence of canine cardiac calsequestrin deduced by cDNA cloning. Journal of Biological Chemistry 263, 8958-8964.
34. 2+ exchanger in end-stage human heart failure. Circulation Research 75, 443-453.
35. THE CARDIAC ARRHYTHMIA SUPPRESSION TRIAL II INVESTIGATORS. (1992). Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. New England Journal of Medicine 327, 227-233.
36. THURINGER, D., DEROUBAIX, E., COULOMBE, A., CORABOEUF, E. & MERCADIER, J. J. (1996). Ionic basis of the action potential prolongation in ventricular myocytes from Syrian hamsters with dilated cardiomyopathy. Cardiovascular Research 31, 747-757.
37. TOMASELLI, G. F., BEUCKELMANN, D. J., CALKINS, H. G., BERGER, R. D., KESSLER, P. D., LAWRENCE, J. H., KASS, D., FELDMAN, A. M. & MARBAN, E. (1994). Sudden cardiac death in heart failure. The role of abnormal repolarization. Circulation 90, 2534-2539.
38. WINSLOW, R. L., RICE, J., JAFRI, S., MARBAN, E. & O'ROURKE, B. (1999). Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, II: model studies. Circulation Research 84, 571-586.