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Cardiovascular Research 2006 69(4):855-864; doi:10.1016/j.cardiores.2005.11.019
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Copyright © 2005, European Society of Cardiology

OxLDL enhances L-type Ca2+ currents via lysophosphatidylcholine-induced mitochondrial reactive oxygen species (ROS) production

Ian M. Fearon*

Faculty of Life Sciences, The University of Manchester, G.38 Stopford Building, Oxford Road, Manchester, M13 9PT, UK

* Tel.: +44 161 275 5496; fax: +44 161 275 5600. Email address: ian.fearon{at}manchester.ac.uk

Objective: To examine the mechanisms underlying oxidised LDL- (oxLDL)-induced alterations in Ca2+ currents, an effect which underlies altered vascular contractility and cardiac myocyte function.

Methods: Ca2+ currents (ICa) were recorded by whole-cell patch-clamp in HEK293 cells expressing L-type Ca2+ channel {alpha}1C subunits or isolated rat ventricular myocytes. oxLDL (but not native LDL) significantly enhanced recombinant ICa, an effect mimicked by 1 µM lysophosphatidylcholine (LPC). LPC failed to enhance ICa either in mitochondrial electron transport chain-depleted {rho}0 cells, or in the presence of rotenone (1 µM), or MPP+ (10 µM). The LPC response was similarly ablated by ascorbate (200 µM) or TROLOX (500 µM) and by the mitochondria-targeted antioxidant, MitoQ (250 nM). In myocytes, enhancement of ICa due to LPC was similarly abrogated with rotenone and MitoQ. These data suggest that LPC enhanced recombinant Ca2+ currents due to increased mitochondrial ROS production. In support with this, LPC enhanced fluorescence in HEK293 cells and cardiac myocytes loaded with a ROS-sensitive mitochondrial dye, reduced mitotracker red.

Conclusion: LPC up-regulates L-type Ca2+ currents due to altered mitochondrial ROS production, an effect which mediates the response of the native ICa in cardiac myocytes to oxLDL.

KEYWORDS Ca-channel; Mitochondria; Lipoproteins; Oxygen radicals

Time for primary review 15 days


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