The Korean Journal of Physiology and Pharmacology

The Korean Society of Pharmacology (대한약리학회)
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Lysophosphatidylcholine Increases $Ca^{2+}$ Current via Activation of Protein Kinase C in Rabbit Portal Vein Smooth Muscle Cells

  • Jung, Seung-Soo (Department of Physiology, Yonsei University College of Medicine) ;
  • Lee, Young-Ho (Department of Physiology, Yonsei University College of Medicine) ;
  • Han, Sung-Sik (Department of Physiology, Yonsei University College of Medicine) ;
  • Kim, Young-Whan (Department of Physiology, Yonsei University College of Medicine) ;
  • Nam, Taik-Sang (Department of Physiology, Yonsei University College of Medicine) ;
  • Ahn, Duck-Sun (Department of Physiology, Yonsei University College of Medicine)
  • Published : 2008.02.28
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Abstract

Lysophosphatidylcholine (LPC), a metabolite of membrane phospholipids by phospholipase $A_2$, has been considered responsible for the development of abnormal vascular reactivity during atherosclerosis. $Ca^{2+}$ influx was shown to be augmented in atherosclerotic artery which might be responsible for abnormal vascular reactivity. However, the mechanism underlying $Ca^{2+}$ influx change in atherosclerotic artery remains undetermined. The purpose of the present study was to examine the effects of LPC on L-type $Ca^{2+}$ current $(I_{Ca(L)})$ activity and to elucidate the mechanism of LPC-induced change of $I_{Ca(L)}$ in rabbit portal vein smooth muscle cells using whole cell patch clamp. Extracellular application of LPC increased $I_{Ca(L)}$ through whole test potentials, and this effect was readily reversed by washout. Steady state voltage dependency of activation or inactivation properties of $I_{Ca(L)}$ was not significantly changed by LPC. Staurosporine (100 nM) or chelerythrine $(3{\mu}M)$, which is a potent inhibitor of PKC, significantly decreased basal $I_{Ca(L)}$, and LPC-induced increase of $I_{Ca(L)}$ was significantly suppressed in the presence of PKC inhibitors. On the other hand, application of PMA, an activator of PKC, increased basal $I_{Ca(L)}$ significantly, and LPC-induced enhancement of $I_{Ca(L)}$ was abolished by pretreatment of the cells with PMA. These findings suggest that LPC increased $I_{Ca(L)}$ in vascular smooth muscle cells by a pathway that involves PKC, and that LPC-induced increase of $I_{Ca(L)}$ might be, at least in part, responsible for increased $Ca^{2+}$ influx in atherosclerotic artery.

Keywords

References

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