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Start Over Author "Roos, Kenneth P" Journal circulation research
12 results on '"Roos, Kenneth P"'

7. Functional Adult Myocardium in the Absence of Na + -Ca 2+ Exchange

Author

Henderson, Scott A., primary, Goldhaber, Joshua I., additional, So, Jessica M., additional, Han, Tieyan, additional, Motter, Christi, additional, Ngo, An, additional, Chantawansri, Chana, additional, Ritter, Matthew R., additional, Friedlander, Martin, additional, Nicoll, Debora A., additional, Frank, Joy S., additional, Jordan, Maria C., additional, Roos, Kenneth P., additional, Ross, Robert S., additional, and Philipson, Kenneth D., additional

Published
2004
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10. Abstract 314.

Author

Parvatiyar, Michelle S, Marshall, Jamie L, Jordan, Maria C, Nguyen, Reginald T, Roos, Kenneth P, and Crosbie-Watson, Rachelle H

Published
2014

11. Abstract 13.

Author

Nakano, Austin, Nakashima, Yasuhiro, Yanez, Diana A, Touma, Marlin, Nakano, Haruko, Jarodzewicz, Artur, Jordan, Maria C, Pellegrini, Matteo, and Roos, Kenneth P

Published
2014

12. Functional adult myocardium in the absence of Na+-Ca2+ exchange: cardiac-specific knockout of NCX1.

Author

Henderson SA, Goldhaber JI, So JM, Han T, Motter C, Ngo A, Chantawansri C, Ritter MR, Friedlander M, Nicoll DA, Frank JS, Jordan MC, Roos KP, Ross RS, and Philipson KD

Subjects
Action Potentials, Adaptation, Physiological, Animals, Calcium Signaling, Echocardiography, Exons genetics, Female, Fetal Heart physiopathology, Gene Targeting, Integrases genetics, Integrases physiology, Male, Mice, Mice, Knockout, Models, Molecular, Myocardial Contraction, Myocardium metabolism, Myocytes, Cardiac metabolism, Myocytes, Cardiac ultrastructure, Patch-Clamp Techniques, Sarcoplasmic Reticulum physiology, Sequence Deletion, Sodium-Calcium Exchanger chemistry, Sodium-Calcium Exchanger genetics, Viral Proteins genetics, Viral Proteins physiology, Heart physiopathology, Sodium-Calcium Exchanger physiology
Abstract

The excitation-contraction coupling cycle in cardiac muscle is initiated by an influx of Ca2+ through voltage-dependent Ca2+ channels. Ca2+ influx induces a release of Ca2+ from the sarcoplasmic reticulum and myocyte contraction. To maintain Ca2+ homeostasis, Ca2+ entry is balanced by efflux mediated by the sarcolemmal Na+-Ca2+ exchanger. In the absence of Na+-Ca2+ exchange, it would be expected that cardiac myocytes would overload with Ca2+. Using Cre/loxP technology, we generated mice with a cardiac-specific knockout of the Na+-Ca2+ exchanger, NCX1. The exchanger is completely ablated in 80% to 90% of the cardiomyocytes as determined by immunoblot, immunofluorescence, and exchange function. Surprisingly, the NCX1 knockout mice live to adulthood with only modestly reduced cardiac function as assessed by echocardiography. At 7.5 weeks of age, measures of contractility are decreased by 20% to 30%. We detect no adaptation of the myocardium to the absence of the Na+-Ca2+ exchanger as measured by both immunoblots and microarray analysis. Ca2+ transients of isolated myocytes from knockout mice display normal magnitudes and relaxation kinetics and normal responses to isoproterenol. Under voltage clamp conditions, the current through L-type Ca2+ channels is reduced by 50%, although the number of channels is unchanged. An abbreviated action potential may further reduce Ca2+ influx. Rather than upregulate other Ca2+ efflux mechanisms, the myocardium appears to functionally adapt to the absence of the Na+-Ca2+ exchanger by limiting Ca2+ influx. The magnitude of Ca2+ transients appears to be maintained by an increased gain of sarcoplasmic reticular Ca2+ release. The myocardium of the NCX1 knockout mice undergoes a remarkable adaptation to maintain near normal cardiac function.

Published
2004
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