TAILIEUCHUNG - Báo cáo khoa học: Mapacalcine specifically blocks hypoxia-induced calcium influx in rat hepatocytes

Post ischaemic cell calcium invasion has been described as one of the main causes of graft failure. Protective effects of calcium antagonists have been investigated but are not con-vincing and their mechanisms of action remain unclear. In this work we tested the protective effect of a new calcium inhibitor described to block a calcium current insensitive to all known calcium blockers. Specific mapacalcine receptors were first characterized on rat hepatocytesmembranes using the 125 I-labeledmapacalcine | Eur. J. Biochem. 270 1952-1957 2003 FEBS 2003 doi Mapacalcine specifically blocks hypoxia-induced calcium influx in rat hepatocytes Dominique Crenesse1 Ghislaine Neuilly2 Jean Gugenheim3 Catherine Ferre1 and Michel Hugues2 1Laboratoire de Physiologie Faculte de Médecine Nice France 2 CNRS UMR 5017 Faculte de Pharmacie Université de Bordeaux 2 France 3Laboratoire de chirurgie experimentale Faculte de Medecine Nice France Post ischaemic cell calcium invasion has been described as one of the main causes of graft failure. Protective effects of calcium antagonists have been investigated but are not convincing and their mechanisms of action remain unclear. In this work we tested the protective effect of a new calcium inhibitor described to block a calcium current insensitive to all known calcium blockers. Specific mapacalcine receptors were first characterized on rat hepatocytes membranes using the 125I-labeled mapacalcine. 45Ca fluxes were then measured on cultured hepatocytes submitted or not to an hypoxic period. The action of mapacalcine was investigated on the ischaemia-induced calcium influx. We demonstrate here that a there are specific receptors for mapacalcine in rat hepatocytes b Mapacalcine is able to specifically block ischaemia-induced calcium influx with an IC50 of M and does not significantly interact with the basal calcium flux. Our work demonstrates that the mapacalcine receptor is a cellular structure directly involved in the phenomenon of postischaemic cell invasion by calcium. Specific block of ischaemia-induced Ca2 influx by mapacalcine suggests that the development of a panel of pharmacological drugs acting on this receptor could lead to the discovery of therapeutic agents able to protect cells against one of the events responsible for organ failure after transplantation or simply after an ischaemic period. Moreover identification of the cellular protein which binds mapacalcine may become an important step in the

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