Laboratory for Physiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands.
Am J Physiol Heart Circ Physiol. 2013 Jan 15;304(2):H260-8. doi: 10.1152/ajpheart.00498.2012. Epub 2012 Nov 9.
PKA-mediated phosphorylation of contractile proteins upon β-adrenergic stimulation plays an important role in the regulation of cardiac performance. Phosphorylation of the PKA sites (Ser(23)/Ser(24)) of cardiac troponin (cTn)I results in a decrease in myofilament Ca(2+) sensitivity and an increase in the rate of relaxation. However, the relation between the level of phosphorylation of the sites and the functional effects in the human myocardium is unknown. Therefore, site-directed mutagenesis was used to study the effects of phosphorylation at Ser(23) and Ser(24) of cTnI on myofilament function in human cardiac tissue. Serines were replaced by aspartic acid (D) or alanine (A) to mimic phosphorylation and dephosphorylation, respectively. cTnI-DD mimics both sites phosphorylated, cTnI-AD mimics Ser(23) unphosphorylated and Ser(24) phosphorylated, cTnI-DA mimics Ser(23) phosphorylated and Ser(24) unphosphorylated, and cTnI-AA mimics both sites unphosphorylated. Force development was measured at various Ca(2+) concentrations in permeabilized cardiomyocytes in which the endogenous troponin complex was exchanged with these recombinant human troponin complexes. In donor cardiomyocytes, myofilament Ca(2+) sensitivity (pCa(50)) was significantly lower in cTnI-DD (pCa(50): 5.39 ± 0.01) compared with cTnI-AA (pCa(50): 5.50 ± 0.01), cTnI-AD (pCa(50): 5.48 ± 0.01), and cTnI-DA (pCa(50): 5.51 ± 0.01) at ~70% cTn exchange. No effects were observed on the rate of tension redevelopment. In cardiomyocytes from idiopathic dilated cardiomyopathic tissue, a linear decline in pCa(50) with cTnI-DD content was observed, saturating at ~55% bisphosphorylation. Our data suggest that in the human myocardium, phosphorylation of both PKA sites on cTnI is required to reduce myofilament Ca(2+) sensitivity, which is maximal at ~55% bisphosphorylated cTnI. The implications for in vivo cardiac function in health and disease are detailed in the DISCUSSION in this article.
PKA 介导的β-肾上腺素能刺激下的收缩蛋白磷酸化在心脏功能调节中起着重要作用。心肌肌钙蛋白 I(cTn)的 PKA 位点(Ser(23)/Ser(24))的磷酸化导致肌丝 Ca2+敏感性降低和松弛速度增加。然而,在人类心肌中,这些位点的磷酸化水平与功能效应之间的关系尚不清楚。因此,使用定点突变来研究 cTnI 上 Ser(23)和 Ser(24)位点的磷酸化对人心肌肌丝功能的影响。丝氨酸被天冬氨酸(D)或丙氨酸(A)取代,分别模拟磷酸化和去磷酸化。cTnI-DD 模拟两个位点磷酸化,cTnI-AD 模拟 Ser(23)未磷酸化和 Ser(24)磷酸化,cTnI-DA 模拟 Ser(23)磷酸化和 Ser(24)未磷酸化,cTnI-AA 模拟两个位点未磷酸化。在将内源性肌钙蛋白复合物交换为这些重组人肌钙蛋白复合物的通透性心肌细胞中,在各种 Ca2+浓度下测量力的发展。在供体心肌细胞中,与 cTnI-AA(pCa(50):5.50 ± 0.01)相比,cTnI-DD(pCa(50):5.39 ± 0.01)中肌丝 Ca2+敏感性(pCa(50))显着降低),cTnI-AD(pCa(50):5.48 ± 0.01)和 cTnI-DA(pCa(50):5.51 ± 0.01),在 ~70%肌钙蛋白交换时。在张力再发展的速度上没有观察到影响。在特发性扩张型心肌病组织的心肌细胞中,随着 cTnI-DD 含量的增加,pCa(50)呈线性下降,在 ~55%双磷酸化时饱和。我们的数据表明,在人类心肌中,cTnI 上的两个 PKA 位点的磷酸化对于降低肌丝 Ca2+敏感性是必需的,在 ~55%双磷酸化的 cTnI 时达到最大值。本文的讨论详细说明了在健康和疾病状态下对体内心脏功能的影响。