Literature DB >> 24080940

Age sensitivity of NFκB abundance and programmed cell death in erythrocytes induced by NFκB inhibitors.

Mehrdad Ghashghaeinia1, Judith C Cluitmans, Mahmoud Toulany, Mohammad Saki, Martin Köberle, Elisabeth Lang, Peter Dreischer, Tilo Biedermann, Michael Duszenko, Florian Lang, Giel J Bosman, Thomas Wieder.   

Abstract

BACKGROUND/AIMS: Erythrocytes may enter eryptosis, a suicidal death characterized by cell shrinkage and phosphatidylserine exposure at the erythrocyte outer membrane. Susceptibility to eryptosis is enhanced in aged erythrocytes and stimulated by NFκB-inhibitors Bay 11-7082 and parthenolide. Here we explored whether expression of NFκB and susceptibility to inhibitor-induced eryptosis is sensitive to erythrocyte age.
METHODS: Human erythrocytes were separated into five fractions, based on age-associated characteristics cell density and volume. NFκB compared to ß-actin protein abundance was estimated by Western blotting and cell volume from forward scatter. Phosphatidylserine exposure was identified using annexin-V binding.
RESULTS: NFκB was most abundant in young erythrocytes but virtually absent in aged erythrocytes. A 24h or 48h exposure to Ringer resulted in spontaneous decrease of forward scatter and increase of annexin V binding, effects more pronounced in aged than in young erythrocytes. Both, Bay 11-7082 (20 µM) and parthenolide (100 µM) triggered eryptosis, effects again most pronounced in aged erythrocytes.
CONCLUSION: NFκB protein abundance is lowest and spontaneous eryptosis as well as susceptibility to Bay 11-7082 and parthenolide highest in aged erythrocytes. Thus, inhibition of NFκB signalling alone is not responsible for the stimulation of eryptosis by parthenolide or Bay 11-7082.
© 2013 S. Karger AG, Basel

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Year:  2013        PMID: 24080940     DOI: 10.1159/000354481

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


  20 in total

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