Phospholipase D increases cell surface Ca2+ binding and positive inotropy in rat heart.
Phospholipase D increases cell surface Ca2+ binding and positive inotropy in rat heart.
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磷脂酶 D 增加大鼠心脏细胞表面 Ca2+ 结合和正性肌力。
DOI：
10.1152/ajpheart.1984.247.5.h880
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Langer,GA
中科院分区：
文献类型：
--
作者：
Burt,JM;Rich,TL;Langer,GA
肌膜中阴离子磷脂(AP)含量的增加可能导致钙结合增加和伴随的变力反应。为了验证这一假设，我们用磷脂酶D(PLD)处理培养的新生大鼠心肌细胞，磷脂酶D是一种将膜磷脂转化为磷脂酸的酶。PLD处理使土壤可交换钙总量增加36%，即1.56+/-0.27 mmolCa+/kg干重，其中79+/-3%可被La3+置换。被多粘菌素B(一种优先取代阴离子磷脂部位的钙离子的药物)置换的钙离子量增加了85%，从预测的0.74+/-0.07增加到1.37+/-0.19 mmolCa+/kg干重量。同时，新生大鼠心室组织的收缩能力增加了1.7-2.5倍。处理细胞的自发性电活动没有明显改变。因此，PLD处理增加了膜上AP的数量，导致AP结合的Ca~(2+)增加了85%，并伴随着显著的收缩作用。目前的结果，与已发表的关于PLD对Na+-Ca~(2+)交换影响的结果相联系(J.Biol。化学。259：16-19,1984)，表明钙离子与肌膜上的阴离子磷脂结合对跨肌膜钙流量和肌力的发展起着重要的控制作用。
An increase in the content of anionic phospholipid (AP) in the sarcolemma may lead to increased Ca2+ binding and a concomitant inotropic response. To test this hypothesis we treated cultured neonatal rat myocardial cells with phospholipase D (PLD), an enzyme that converts membrane phospholipids to phosphatidic acid. PLD treatment resulted in an increase in total exchangeable Ca2+ of 36%, or 1.56 +/- 0.27 mmol Ca2+/kg dry wt, 79 +/- 3% of which remained displaceable by La3+. The quantity of Ca2+ displaced by polymyxin B, a drug that displaces Ca2+ preferentially from anionic phospholipid sites, increased by 85% from a predicted 0.74 +/- 0.07 to 1.37 +/- 0.19 mmol Ca2+/kg dry wt. Simultaneously the contractility of neonatal rat ventricular tissue increased by 1.7- to 2.5-fold. Spontaneous electrical activity of treated cells was not significantly altered. Thus PLD treatment, which increases the quantity of AP in the membrane, resulted in an 85% increase in Ca2+ bound to AP and concomitantly resulted in a significant increase in contractility. Present results, in association with published results on the effect of PLD on Na+-Ca2+ exchange (J. Biol. Chem. 259: 16-19, 1984), indicate that Ca2+ bound to anionic sarcolemmal phospholipids plays a major role in the control of transsarcolemmal Ca2+ flux and force development.