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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Lysophosphatidylcholine Increases Ca2+ Current via Activation of Protein Kinase C in Rabbit Portal Vein Smooth Muscle Cells
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Lysophosphatidylcholine Increases Ca2+ Current via Activation of Protein Kinase C in Rabbit Portal Vein Smooth Muscle Cells

机译：溶血磷脂酰胆碱通过激活兔门静脉平滑肌细胞中的蛋白激酶C来增加Ca2 +电流。

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Lysophosphatidylcholine (LPC), a metabolite of membrane phospholipids by phospholipase A2, has been considered responsible for the development of abnormal vascular reactivity during atherosclerosis. Ca2+ influx was shown to be augmented in atherosclerotic artery which might be responsible for abnormal vascular reactivity. However, the mechanism underlying Ca2+ influx change in atherosclerotic artery remains undetermined. The purpose of the present study was to examine the effects of LPC on L-type Ca2+ current (ICa(L)) activity and to elucidate the mechanism of LPC-induced change of ICa(L) in rabbit portal vein smooth muscle cells using whole cell patch clamp. Extracellular application of LPC increased ICa(L) through whole test potentials, and this effect was readily reversed by washout. Steady state voltage dependency of activation or inactivation properties of ICa(L) was not significantly changed by LPC. Staurosporine (100 nM) or chelerythrine (3 μM), which is a potent inhibitor of PKC, significantly decreased basal ICa(L), and LPC-induced increase of ICa(L) was significantly suppressed in the presence of PKC inhibitors. On the other hand, application of PMA, an activator of PKC, increased basal ICa(L) significantly, and LPC-induced enhancement of ICa(L) was abolished by pretreatment of the cells with PMA. These findings suggest that LPC increased ICa(L) in vascular smooth muscle cells by a pathway that involves PKC, and that LPC-induced increase of ICa(L) might be, at least in part, responsible for increased Ca2+ influx in atherosclerotic artery.
机译：溶血磷脂酰胆碱（LPC）是磷脂酶A 2 的膜磷脂代谢产物，被认为是动脉粥样硬化期间异常血管反应性发展的原因。 Ca 2 + 内流在动脉粥样硬化动脉中增加，这可能是导致血管反应异常的原因。然而，动脉粥样硬化动脉中Ca 2 + 流入变化的机制仍未确定。本研究的目的是研究LPC对L型Ca 2 + 电流（I Ca（L））活性的影响，并阐明LPC的机制。全细胞膜片钳诱导家兔门静脉平滑肌细胞中I Ca（L）的变化在整个测试电位下，LPC的细胞外施用增加了I Ca（L），并且这种作用很容易被冲蚀逆转。 LPC对I Ca（L）的活化或失活性质的稳态电压依赖性没有显着改变。 Staurosporine（100 nM）或白屈菜红碱（3μM）是一种有效的PKC抑制剂，可显着降低基础I Ca（L），并且LPC诱导的I Ca（L）升高在存在PKC抑制剂的情况下被显着抑制。另一方面，PKA的活化剂PMA的使用显着增加了基础I Ca（L）的含量，并且废除了LPC诱导的I Ca（L）的增强作用通过用PMA预处理细胞。这些发现表明LPC通过涉及PKC的途径增加了血管平滑肌细胞中的I Ca（L），并且LPC诱导的I Ca（L）的增加可能至少部分是造成动脉粥样硬化动脉Ca 2 + 流入增加的原因。

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