| First Author | Brickson S | Year | 2007 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 292 |
| Issue | 4 | Pages | H1747-54 |
| PubMed ID | 17122190 | Mgi Jnum | J:125829 |
| Mgi Id | MGI:3760017 | Doi | 10.1152/ajpheart.01037.2006 |
| Citation | Brickson S, et al. (2007) In vivo left ventricular functional capacity is compromised in cMyBP-C null mice. Am J Physiol Heart Circ Physiol 292(4):H1747-54 |
| abstractText | Cardiac myosin binding protein-C (cMyBP-C) is a thick filament-associated protein that binds tightly to myosin and has a potential role for modulating myocardial contraction. We tested the hypothesis that cMyBP-C 1) contributes to the enhanced in vivo contractile state following beta-adrenergic stimulation and 2) is necessary for myocardial adaptation to chronic increases in afterload. In vivo pressure-volume relations demonstrated that left ventricular (LV) systolic and diastolic function were compromised under basal conditions in cMyBP-C(-/-) compared with WT mice. Moreover, whereas beta-adrenergic treatment significantly improved ejection fraction, peak elastance, and the time to peak elastance in WT mice, these functional indexes remained unchanged in cMyBP-C(-/-) mice. Morphological and functional changes were measured through echocardiography in anesthetized mice following 5 wk of aortic banding. Adaptation to pressure overload was diminished in cMyBP-C(-/-) mice as characterized by a lack of an increase in posterior wall thickness, increased LV diameter, deterioration of fractional shortening, and prolonged isovolumic relaxation time. These results suggest that the absence of cMyBP-C significantly diminishes in vivo LV function and markedly attenuates the increase in LV contractility following beta-adrenergic stimulation or adaptation to pressure overload. |
