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Enhanced suicidal erythrocyte death in mice carrying a loss-of-function mutation of the adenomatous polyposis coli gene.

Qadri SM, Mahmud H, Lang E, Gu S, Bobbala D, Zelenak C, Jilani K, Siegfried A, Föller M, Lang F - J. Cell. Mol. Med. (2012)

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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, University of Tübingen, Tübingen, Germany.

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Enhanced phosphatidylserine abundance at the surface of erythrocytes from APC-deficient mice. (A) Histogram of annexin V binding reflecting phosphatidylserine exposure in a representative experiment of erythrocytes from APC-deficient mice (apcMin/+) and their wild-type littermates (apc+/+) exposed for 8 hrs to glucose-depleted Ringer. (B) Arithmetic mean ± S.E.M. (n = 4) of the percentage of annexin V-binding erythrocytes from 8-week-old APC-deficient mice (apcMin/+, black bars) and wild-type mice (apc+/+, white bars) exposed for 8 hrs to glucose-containing (left bars) or glucose-depleted (right bars) Ringer. Annexin V bound to the cell membrane whereas CFSE accumulated in the cytosol. * indicates significant (P < 0.05) difference from glucose-containing Ringer; # indicates significant difference (P < 0.05) between genotypes (Mann–Whitney test).
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fig03: Enhanced phosphatidylserine abundance at the surface of erythrocytes from APC-deficient mice. (A) Histogram of annexin V binding reflecting phosphatidylserine exposure in a representative experiment of erythrocytes from APC-deficient mice (apcMin/+) and their wild-type littermates (apc+/+) exposed for 8 hrs to glucose-depleted Ringer. (B) Arithmetic mean ± S.E.M. (n = 4) of the percentage of annexin V-binding erythrocytes from 8-week-old APC-deficient mice (apcMin/+, black bars) and wild-type mice (apc+/+, white bars) exposed for 8 hrs to glucose-containing (left bars) or glucose-depleted (right bars) Ringer. Annexin V bound to the cell membrane whereas CFSE accumulated in the cytosol. * indicates significant (P < 0.05) difference from glucose-containing Ringer; # indicates significant difference (P < 0.05) between genotypes (Mann–Whitney test).

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 [34]. 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.


Enhanced suicidal erythrocyte death in mice carrying a loss-of-function mutation of the adenomatous polyposis coli gene.

Qadri SM, Mahmud H, Lang E, Gu S, Bobbala D, Zelenak C, Jilani K, Siegfried A, Föller M, Lang F - J. Cell. Mol. Med. (2012)

Enhanced phosphatidylserine abundance at the surface of erythrocytes from APC-deficient mice. (A) Histogram of annexin V binding reflecting phosphatidylserine exposure in a representative experiment of erythrocytes from APC-deficient mice (apcMin/+) and their wild-type littermates (apc+/+) exposed for 8 hrs to glucose-depleted Ringer. (B) Arithmetic mean ± S.E.M. (n = 4) of the percentage of annexin V-binding erythrocytes from 8-week-old APC-deficient mice (apcMin/+, black bars) and wild-type mice (apc+/+, white bars) exposed for 8 hrs to glucose-containing (left bars) or glucose-depleted (right bars) Ringer. Annexin V bound to the cell membrane whereas CFSE accumulated in the cytosol. * indicates significant (P < 0.05) difference from glucose-containing Ringer; # indicates significant difference (P < 0.05) between genotypes (Mann–Whitney test).
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Related In: Results  -  Collection

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fig03: Enhanced phosphatidylserine abundance at the surface of erythrocytes from APC-deficient mice. (A) Histogram of annexin V binding reflecting phosphatidylserine exposure in a representative experiment of erythrocytes from APC-deficient mice (apcMin/+) and their wild-type littermates (apc+/+) exposed for 8 hrs to glucose-depleted Ringer. (B) Arithmetic mean ± S.E.M. (n = 4) of the percentage of annexin V-binding erythrocytes from 8-week-old APC-deficient mice (apcMin/+, black bars) and wild-type mice (apc+/+, white bars) exposed for 8 hrs to glucose-containing (left bars) or glucose-depleted (right bars) Ringer. Annexin V bound to the cell membrane whereas CFSE accumulated in the cytosol. * indicates significant (P < 0.05) difference from glucose-containing Ringer; # indicates significant difference (P < 0.05) between genotypes (Mann–Whitney test).
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 [34]. 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.

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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, University of Tübingen, Tübingen, Germany.

Show MeSH
Related in: MedlinePlus