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Korean Society for Biochemistry and Molecular Biology (생화학분자생물학회)
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Effects of chlorogenic acid on intracellular calcium regulation in lysophosphatidylcholine-treated endothelial cells

  • Jung, Hye-Jin (Department of Physiology, Keimyung University School of Medicine) ;
  • Im, Seung-Soon (Department of Physiology, Keimyung University School of Medicine) ;
  • Song, Dae-Kyu (Department of Physiology, Keimyung University School of Medicine) ;
  • Bae, Jae-Hoon (Department of Physiology, Keimyung University School of Medicine)
  • Received : 2016.10.25
  • Accepted : 2017.01.10
  • Published : 2017.06.30
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Abstract

Lysophosphatidylcholine (LPC) is a major phospholipid component of oxidized low-density lipoprotein (ox-LDL) and is implicated in its atherogenic activity. This study investigated the effects of LPC on cell viability, intracellular calcium homeostasis, and the protective mechanisms of chlorogenic acid (CGA) in human umbilical vein endothelial cells (HUVECs). LPC increased intracellular calcium ($[Ca^{2+}]_i$) by releasing $Ca^{2+}$ from intracellular stores and via $Ca^{2+}$ influx through store-operated channels (SOCs). LPC also increased the generation of reactive oxygen species (ROS) and decreased cell viability. The mRNA expression of Transient receptor potential canonical (TRPC) channel 1 was increased significantly by LPC treatment and suppressed by CGA. CGA inhibited LPC-induced $Ca^{2+}$ influx and ROS generation, and restored cell viability. These results suggested that CGA inhibits SOC-mediated $Ca^{2+}$ influx and ROS generation by attenuating TRPC1 expression in LPC-treated HUVECs. Therefore, CGA might protect endothelial cells against LPC injury, thereby inhibiting atherosclerosis.

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References

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