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Modulation of nonselective cation current by oxidized LDL and lysophosphatidylcholine and its inhibitory contribution to endothelial damage

Title
Modulation of nonselective cation current by oxidized LDL and lysophosphatidylcholine and its inhibitory contribution to endothelial damage
Authors
Liang G.H.Park S.Kim M.Y.Kim J.A.Choi S.Suh S.H.
Ewha Authors
서석효최신규박성희
SCOPUS Author ID
서석효scopus; 최신규scopus; 박성희scopus
Issue Date
2010
Journal Title
Life Sciences
ISSN
0024-3205JCR Link
Citation
vol. 86, no. 19-20, pp. 733 - 739
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
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.
DOI
10.1016/j.lfs.2010.03.005
Appears in Collections:
의과대학 > 의학과 > Journal papers
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