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- Title
Induction of Suicidal Erythrocyte Death by Novobiocin.
- Authors
Lupescu, Adrian; Bissinger, Rosi; Herrmann, Tabea; Oswald, Gergely; Jilani, Kashif; Lang, Florian
- Abstract
Background: Novobiocin, an aminocoumarin antibiotic, interferes with heat shock protein 90 and hypoxia inducible factor dependent gene expression and thus compromises cell survival. Similar to survival of nucleated cells, erythrocyte survival could be disrupted by eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and by phospholipd scrambling of the cell membrane with phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca2+-activity ([Ca2+]i). The Ca2+ sensitivity of phospholipid scrambling is enhanced by ceramide. The present study explored, whether novobiocin elicits eryptosis. Methods: [Ca2+]i was estimated from Fluo3-fluorescence, ceramide abundance utilizing fluorescent antibodies, cell volume from forward scatter, phosphatidylserine-exposure from annexin V binding. Results: A 48 hours exposure to novobiocin (500 µM) was followed by a significant increase of [Ca2+]i, decrease of forward scatter, increase of annexin-V-binding and enhanced ceramide formation. Removal of extracellular Ca2+ virtually abrogated the increase of annexin-V-binding following novobiocin exposure. Conclusions: Novobiocin stimulates eryptosis, an effect at least in part due to entry of extracellular Ca2+ and formation of ceramide. © 2014 S. Karger AG, Basel
- Subjects
ERYTHROCYTES; NOVOBIOCIN; ANTIBIOTICS; HEAT shock proteins; HYPOXIA-inducible factors; GENE expression; PHOSPHATIDYLSERINES; PHYSIOLOGY
- Publication
Cellular Physiology & Biochemistry (Karger AG), 2014, Vol 33, Issue 3, p670
- ISSN
1015-8987
- Publication type
Article
- DOI
10.1159/000358643