Luo W, Wolska B M, Grupp I L, Harrer J M, Haghighi K, Ferguson D G, Slack J P, Grupp G, Doetschman T, Solaro R J, Kranias E G
Department of Pharmacology, University of Cincinnati, College of Medicine, Ohio 45267-0575, USA.
Circ Res. 1996 May;78(5):839-47. doi: 10.1161/01.res.78.5.839.
Phospholamban ablation has been shown to result in significant increases in cardiac contractile parameters and loss of beta-adrenergic stimulation. To determine whether partial reduction in phospholamban levels is also associated with enhancement of cardiac performance and to further examine the sensitivity of the contractile system to alterations in phospholamban levels, hearts from wild-type, phospholamban-heterozygous, and phospholamban-deficient mice were studied in parallel at the subcellular, cellular, and organ levels. The phospholamban-heterozygous mice expressed reduced cardiac phospholamban mRNA and protein levels (40 +/- 5%) compared with wild type mice. The reduced phospholamban levels were associated with significant decreases in the EC50 of the sarcoplasmic reticulum Ca2+ pump for CA2+ and increases in the contractile parameters of isolated myocytes and beating hearts. The relative phospholamban levels among wild-type, phospholamban-heterozygous, and phospholamban-deficient mouse hearts correlated well with the (1) EC50 of the Ca(2+)-ATPase for Ca2+ in sarcoplasmic reticulum, (2) rates of relaxation and contraction in isolated cardiac myocytes, and (3) rates of relaxation and intact beating hearts. These findings suggest that physiological and pathological changes in the levels of phospholamban will result in parallel changes in sarcoplasmic reticulum function and cardiac contraction.
磷酸受磷蛋白缺失已被证明会导致心脏收缩参数显著增加以及β-肾上腺素能刺激丧失。为了确定磷酸受磷蛋白水平的部分降低是否也与心脏功能增强相关,并进一步研究收缩系统对磷酸受磷蛋白水平变化的敏感性,我们同时在亚细胞、细胞和器官水平对野生型、磷酸受磷蛋白杂合型和磷酸受磷蛋白缺陷型小鼠的心脏进行了研究。与野生型小鼠相比,磷酸受磷蛋白杂合型小鼠心脏中磷酸受磷蛋白的mRNA和蛋白质水平降低(40±5%)。磷酸受磷蛋白水平的降低与肌浆网Ca2+泵对Ca2+的EC50显著降低以及分离的心肌细胞和跳动心脏的收缩参数增加有关。野生型、磷酸受磷蛋白杂合型和磷酸受磷蛋白缺陷型小鼠心脏中磷酸受磷蛋白的相对水平与(1)肌浆网中Ca(2+)-ATP酶对Ca2+的EC50、(2)分离的心肌细胞的舒张和收缩速率以及(3)完整跳动心脏的舒张和收缩速率密切相关。这些发现表明,磷酸受磷蛋白水平的生理和病理变化将导致肌浆网功能和心脏收缩的平行变化。