Oxidized Low-density Lipoprotein- and Lysophosphatidylcholine-induced Ca2+ Mobilization in Human Endothelial Cells.
10.4196/kjpp.2009.13.1.27
- Author:
Moon Young KIM
1
;
Guo Hua LIANG
;
Ji Aee KIM
;
Soo Seung CHOI
;
Shinku CHOI
;
Suk Hyo SUH
Author Information
1. Department of Physiology and Medical Research Institute, School of Medicine, Ewha Womans University, Seoul 158-710, Korea. shsuh@ewha.ac.kr
- Publication Type:Original Article
- Keywords:
Oxidized LDL;
Endothelial cell;
Store-operated Ca2+ entry;
Large conductance Ca2+-activated K+ channel;
Nonselective cation current
- MeSH:
Constriction;
Cyclic N-Oxides;
Endothelial Cells;
Estrenes;
Fluorescence;
Fura-2;
Heparin;
Humans;
Lipoproteins;
Lipoproteins, LDL;
Lysophosphatidylcholines;
Pyrrolidinones;
Sarcoplasmic Reticulum;
Spin Labels
- From:The Korean Journal of Physiology and Pharmacology
2009;13(1):27-32
- CountryRepublic of Korea
- Language:English
-
Abstract:
The effects of oxidized low-density lipoprotein (OxLDL) and its major lipid constituent lysophosphatidylcholine (LPC) on Ca2+ entry were investigated in cultured human umbilical endothelial cells (HUVECs) using fura-2 fluorescence and patch-clamp methods. OxLDL or LPC increased intracellular Ca2+ concentration ([Ca2+]i), and the increase of [Ca2+]i by OxLDL or by LPC was inhibited by La3+ or heparin. LPC failed to increase [Ca2+]i in the presence of an antioxidant tempol. In addition, store-operated Ca2+ entry (SOC), which was evoked by intracellular Ca2+ store depletion in Ca2+-free solution using the sarcoplasmic reticulum Ca2+ pump blocker, 2, 5-di-t-butyl-1, 4-benzohydroquinone (BHQ), was further enhanced by OxLDL or by LPC. Increased SOC by OxLDL or by LPC was inhibited by U73122. In voltage-clamped cells, OxLDL or LPC increased [Ca2+]i and simultaneously activated non-selective cation (NSC) currents. LPC-induced NSC currents were inhibited by 2-APB, La3+ or U73122, and NSC currents were not activated by LPC in the presence of tempol. Furthermore, in voltage-clamped HUVECs, OxLDL enhanced SOC and evoked outward currents simultaneously. Clamping intracellular Ca2+ to 1 micrometer activated large-conductance Ca2+-activated K+ (BKCa) current spontaneously, and this activated BKCa current was further enhanced by OxLDL or by LPC. From these results, we concluded that OxLDL or its main component LPC activates Ca2+-permeable Ca2+-activated NSC current and BKCa current simultaneously, thereby increasing SOC.
