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Melatonin elevates intracellular free calcium in human platelets by inositol 1,4,5‐trisphosphate independent mechanism
Author(s) -
Kumari Sharda,
Dash Debabrata
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.05.067
Subject(s) - melatonin , luzindole , calcium , inositol , calcium in biology , phospholipase c , chemistry , endocrinology , medicine , melatonin receptor , receptor , intracellular , platelet , inositol trisphosphate , inositol trisphosphate receptor , biochemistry , biology
Several studies have indicated the existence of direct effects of melatonin on platelets. Here we show that, melatonin at high concentration is capable of significantly raising platelet intracellular calcium even in the absence of an agonist. The effect of melatonin on platelets was abolished by luzindole, a melatonin receptor blocker, and rotenone, while it was unaffected by cell‐permeable antagonists of either inositol 1,4,5‐trisphosphate (IP 3 ) receptor, phospholipase C (PLC), or bafilomycin A1, which discharges acidic calcium stores. Melatonin‐induced manganese entry provided evidence for activation of bivalent cation entry. Thus, our data suggest that melatonin evoked the elevation of platelet intracellular calcium through depletion of mitochondrial Ca 2+ stores and store‐operated calcium entry (SOCE), while the action was independent of the PLC‐IP 3 axis.