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Eryptosis, a Window to Systemic DiseaseLang F.1 · Gulbins E.2 · Lerche H.3 · Huber S.M.1,4 · Kempe D.S.1 · Föller M.1
1Department of Physiology, University of Tübingen2Department of Molecular Biology, University of Duisburg-Essen3Neurological Clinic and Institute of Applied Physiology, University of Ulm4Department of Radiation Oncology, University of Tübingen Corresponding Author
Prof. Dr. Florian Lang
Physiologisches Institut der Universität Tübingen
Gmelinstr. 5, D-72076 Tübingen (Germany)
Tel. +49 7071 29 72194, Fax: +49 7071 29 5618
Similar to apoptosis of nucleated cells, suicidal erythrocyte death or eryptosis is characterized by cell shrinkage, membrane blebbing and membrane phospholipid scrambling with phosphatidylserine exposure at the cell surface. Signaling of eryptosis involves formation of prostaglandin E2 with subsequent activation of cation channels and Ca2+-entry and/or release of platelet activating factor (PAF) with subsequent activation of sphingomyelinase and formation of ceramide. Ca2+ and ceramide stimulate cell membrane scrambling. Ca2+ further activates Ca2+-sensitive K+-channels leading to cellular KCl loss and cell shrinkage and stimulates the protease calpain resulting in degradation of the cytoskeleton. Injuries triggering eryptosis may similarly compromise survival of nucleated cells. The case is made that analysis of enhanced eryptosis may direct to the pathophysiology of systemic disease. Examples presented include drug side effects, sepsis, haemolytic uremic syndrome, Wilson´s disease, phosphate depletion and a rare condition caused by a mutation in GLUT1 turning the carrier into a cation channel.
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