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Modulation of nonselective cation current by oxidized LDL and lysophosphatidylcholine and its inhibitory contribution to endothelial damage
- Modulation of nonselective cation current by oxidized LDL and lysophosphatidylcholine and its inhibitory contribution to endothelial damage
- Liang G.H.; Park S.; Kim M.Y.; Kim J.A.; Choi S.; Suh S.H.
- Ewha Authors
- 서석효; 최신규; 박성희
- SCOPUS Author ID
- 서석효; 최신규; 박성희
- Issue Date
- Journal Title
- Life Sciences
- vol. 86, no. 19-20, pp. 733 - 739
- SCI; SCIE; SCOPUS
- Aims: This study examined the effects of oxidized low-density lipoprotein (LDL) and its major lipid constituent lysophosphatidylcholine (LPC) on nonselective cation (NSC) current and its inhibitory contribution to LPC-induced cytotoxicity in cultured human umbilical endothelial cells (HUVECs). Main methods: Patch-clamp technique and the resazurin-based cell viability assay were used. Key findings: In voltage-clamped cells, oxidized LDL or LPC slowly activated NSC current. NSC current was also activated by loading cells with Ca2+ solution buffered at various concentrations using a patch pipette or by applying the sarcoplasmic reticulum Ca2+ pump blocker 2,5-di-t-butyl-1,4-benzohydroquinone (BHQ), the metabolic inhibitor CN- or the hydroperoxide donor tert-butyl hydroperoxide (TBHP). On the contrary, when intracellular Ca2+ was strongly buffered with 12mM BAPTA or cells were loaded with superoxide dismutase using a patch pipette, LPC or BHQ did not activate NSC current. Furthermore, NSC current activated by LPC, TBHP or CN- was inhibited by the antioxidant tempol or extracellular Ca2+ depletion and NSC current activated by intracellular Ca2+ was further augmented by oxidized LDL or LPC. LPC or oxidized LDL released Ca2+ from intracellular stores and further enhanced store-operated Ca2+ entry. LPC-induced cytotoxicity was augmented by inhibiting Ca2+ influx and NO synthesis. Significance: Oxidized LDL or its main component LPC activated Ca2+-permeable NSC current via releasing Ca2+ from intracellular stores and producing ROS and thereby increased Ca2+ influx. Ca2+ influx through NSC channel might protect endothelial cells by producing NO. © 2010 Elsevier Inc.
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