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  • Title: Participation of leukotriene C(4) in the regulation of suicidal erythrocyte death.
    Author: Foller M, Mahmud H, Gu S, Wang K, Floride E, Kucherenko Y, Luik S, Laufer S, Lang F.
    Journal: J Physiol Pharmacol; 2009 Sep; 60(3):135-43. PubMed ID: 19826192.
    Abstract:
    Eryptosis, the suicidal death of erythrocytes, is characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine exposure at the erythrocyte surface. Eryptosis is triggered by increase in cytosolic Ca(2+) concentration upon energy depletion. The present study explored the involvement of leukotrienes. Western blotting was employed to detect the cysteinyl-leukotriene receptor cysLT1, competitive immune assay to determine leukotriene release from erythrocytes, Fluo3 fluorescence to estimate cytosolic Ca(2+) concentration, forward scatter to analyse cell volume and annexin V-binding to disclose phosphatidylserine exposure. As a result, erythrocytes expressed the leukotriene receptor CysLT1. Glucose depletion (24 hours) significantly increased the formation of the cysteinyl-leukotrienes C(4)/D(4)/E(4). Leukotriene C(4) (10 nM) increased Ca(2+) entry, decreased forward scatter, activated caspases 3 and 8, and stimulated annexin V-binding. Glucose depletion similarly increased annexin V-binding, an effect significantly blunted in the presence of the leukotriene receptor antagonist cinalukast (1 microM) or the 5-lipoxygenase inhibitor BW B70C (1 microM). In conclusion, upon energy depletion erythrocytes form leukotrienes, which in turn activate cation channels, leading to Ca(2+) entry, cell shrinkage and cell membrane scrambling. Cysteinyl-leukotrienes thus participate in the signaling of eryptosis during energy depletion.
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