Enhanced suicidal erythrocyte death in mice carrying a loss-of-function mutation of the adenomatous polyposis coli gene.
Bottom Line: Glucose depletion enhanced annexin V binding, an effect significantly more pronounced in apc(Min/+) erythrocytes than in apc(+/+) erythrocytes.Extracellular Ca(2+) removal or inhibition of Ca(2+) entry with amiloride (1 mM) blunted the increase but did not abrogate the genotype differences of annexin V binding following glucose depletion.Stimulation of Ca(2+) -entry by treatment with Ca(2+) -ionophore ionomycin (10 μM) increased annexin V binding, an effect again significantly more pronounced in apc(Min/+) erythrocytes than in apc(+/+) erythrocytes.
Affiliation: Department of Physiology, University of Tübingen, Tübingen, Germany.Show MeSH
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Mentions: In view of the accelerated clearance of circulating erythrocytes in the spleen of apcMin/+ mice and their enhanced phosphatidylserine exposure at the cell surface, additional experiments were performed to determine annexin V binding of apcMin/+ erythrocytes and apc+/+ erythrocytes in FACS analysis. The experiments were performed in the presence and absence of glucose, as energy depletion is known to foster eryptosis . As shown in Figure 3A and B, annexin V binding reflecting phosphatidylserine exposure at the erythrocyte surface was significantly higher in apcMin/+ erythrocytes than in apc+/+ erythrocytes following energy depletion.
Affiliation: Department of Physiology, University of Tübingen, Tübingen, Germany.