PGE(2) in the regulation of programmed erythrocyte death.

Lang, P A, Kempe, D S, Mysina, Svetlana, Tanneur, V, Birka, C, Laufer, S, Lang, F, Wieder, T and Huber, S M (2005) PGE(2) in the regulation of programmed erythrocyte death. Cell death and differentiation, 12 (5). pp. 415-28. ISSN 1350-9047

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Abstract

Hyperosmotic shock, energy depletion, or removal of extracellular Cl(-) activates Ca(2+)-permeable cation channels in erythrocyte membranes. Subsequent Ca(2+) entry induces erythrocyte shrinkage and exposure of phosphatidylserine (PS) at the erythrocyte surface. PS-exposing cells are engulfed by macrophages. The present study explored the signalling involved. Hyperosmotic shock and Cl(-) removal triggered the release of prostaglandin E(2) (PGE(2)). In whole-cell recording, activation of the cation channels by Cl(-) removal was abolished by the cyclooxygenase inhibitor diclophenac. In FACS analysis, phospholipase-A(2) inhibitors quinacrine and palmitoyltrifluoromethyl-ketone, and cyclooxygenase inhibitors acetylsalicylic acid and diclophenac, blunted the increase of PS exposure following Cl(-) removal. PGE(2) (but not thromboxane) induced cation channel activation, increase in cytosolic Ca(2+) concentration, cell shrinkage, PS exposure, calpain activation, and ankyrin-R degradation. The latter was attenuated by calpain inhibitors-I/II, while PGE(2)-induced PS exposure was not. In conclusion, hyperosmotic shock or Cl(-) removal stimulates erythrocyte PS exposure through PGE(2) formation and subsequent activation of Ca(2+)-permeable cation channels.

Item Type: Article
Subjects: Sciences > Biomedical Sciences
Depositing User: Svetlana Mysina
Date Deposited: 08 Oct 2018 09:19
Last Modified: 09 Oct 2018 10:28
URI: http://sure.sunderland.ac.uk/id/eprint/10020

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