| First Author | Pott C | Year | 2004 |
| Journal | Biochem Biophys Res Commun | Volume | 322 |
| Issue | 4 | Pages | 1336-40 |
| PubMed ID | 15336980 | Mgi Jnum | J:92483 |
| Mgi Id | MGI:3052895 | Doi | 10.1016/j.bbrc.2004.08.038 |
| Citation | Pott C, et al. (2004) Genetic manipulation of cardiac Na+/Ca2+ exchange expression. Biochem Biophys Res Commun 322(4):1336-40 |
| abstractText | The Na+/Ca2+ exchanger (NCX) is the primary Ca2+ extrusion mechanism in cardiomyocytes. To further investigate the role of NCX in excitation-contraction coupling and Ca2+ homeostasis, we created murine models with altered expression levels of NCX. Homozygous overexpression of NCX resulted in mild cardiac hypertrophy. Decline of the Ca2+ transient and relaxation of contraction were increased and the reverse mode of NCX was augmented. Overexpression also led to a higher susceptibility to ischemia-reperfusion injury and to a greater ability of NCX to trigger Ca2+-induced Ca2+ release. Furthermore, an increase in peak L-type Ca2+ current was observed suggesting a direct influence of NCX on L-type Ca2+ current. Whereas global knockout of NCX led to prenatal death, a recently generated cardiac-specific NCX knockout mouse was viable with surprisingly normal contractile properties. Expression levels of other Ca2+-handling proteins were not altered. Ca2+ influx in these animals is limited by a decrease of peak L-type Ca2+ current. An alternative Ca2+ efflux mechanism, presumably the plasma membrane Ca2+-ATPase, is sufficient to maintain Ca2+-homeostasis in the NCX knockout mice. |
