Prevalence of hypochromia (without microcytosis) vs microcytosis (without hypochromia) in iron deficiency

Jolobe, Oscar M.P.

doi:10.1046/j.1365-2257.2000.00293.x

Cited by 45 publications

(29 citation statements)

References 7 publications

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“…Accordingly, breakdown of phosphatidylserine asymmetry might be important for erythrocyte ageing, which is paralleled by an increase of cytosolic Ca 2+ activity (Romero et al, 1999;Kiefer et al, 2000). Beyond that, any erythrocyte disorder that facilitates cell shrinkage, such as sickle cell anaemia (Joiner, 1993;Wu et al, 2003), thalassaemia (Mach-Pascual et al, 1996) or iron deficiency (Jolobe, 2000), would be expected to favour phosphatidylserine exposure at the erythrocyte surface, an effect which has indeed been observed in a previous study . It is noteworthy that the plasma levels of several pro-inflammatory cytokines, including PAF, are enhanced in sickle cell anemia (Rivera et al, 2002).…”

Section: Discussionmentioning

confidence: 62%

Stimulation of erythrocyte ceramide formation by platelet-activating factor

Lang

Kempe

Tanneur

et al. 2005

Journal of Cell Science

142

126

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Osmotic erythrocyte shrinkage leads to activation of cation channels with subsequent Ca2+ entry and stimulates a sphingomyelinase with subsequent formation of ceramide. Ca2+ and ceramide then activate a scramblase leading to breakdown of phosphatidylserine asymmetry of the cell membrane. The mediators accounting for activation of erythrocyte sphingomyelinase and phosphatidylserine exposure remained elusive. The study demonstrates that platelet-activating factor (PAF) is released from erythrocytes upon hyperosmotic cell shrinkage. The experiments further disclose the presence of PAF receptors in erythrocytes and show that PAF stimulates the breakdown of sphingomyelin and the release of ceramide from erythrocytes at isotonic conditions. PAF further triggers cell shrinkage (decrease of forward scatter) and phosphatidylserine exposure (annexin binding) of erythrocytes. The stimulation of annexin-binding is blunted by a genetic knockout of PAF receptors, by the PAF receptor antagonist ABT491 or by inhibition of sphingomyelinase with urea. In conclusion, PAF activates an erythrocyte sphingomyelinase and the then formed ceramide leads to the activation of scramblase with subsequent phosphatidylserine exposure.

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Section: Discussionmentioning

confidence: 62%

Stimulation of erythrocyte ceramide formation by platelet-activating factor

Lang

Kempe

Tanneur

et al. 2005

Journal of Cell Science

142

126

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“…24 The subsequent erythrocyte apoptosis may then contribute to the derangement of microcirculation. Beyond this any erythrocyte disorder facilitating erythrocyte shrinkage, such as sickle cell disease, 8,25 thalassemia 26 or iron deficiency, 27 could, to the extent as it leads to activation of the cell volume regulatory cation channels, trigger premature apoptosis and thus accelerate erythrocyte death.…”

Section: Discussionmentioning

confidence: 99%

Cation channels trigger apoptotic death of erythrocytes

et al. 2003

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Erythrocytes are devoid of mitochondria and nuclei and were considered unable to undergo apoptosis. As shown recently, however, the Ca 2+ -ionophore ionomycin triggers breakdown of phosphatidylserine asymmetry (leading to annexin binding), membrane blebbing and shrinkage of erythrocytes, features typical for apoptosis in nucleated cells. In the present study, the effects of osmotic shrinkage and oxidative stress, well-known triggers of apoptosis in nucleated cells, were studied. Exposure to 850 mOsm for 24 h, to tert-butylhydroperoxide (1 mM) for 15 min, or to glucose-free medium for 48 h, all elicit erythrocyte shrinkage and annexin binding, both sequelae being blunted by removal of extracellular Ca 2+ and mimicked by ionomycin (1 lM). Osmotic shrinkage and oxidative stress activate Ca 2+ -permeable cation channels and increase cytosolic Ca 2+ concentration. The channels are inhibited by amiloride (1 mM), which further blunts annexin binding following osmotic shock, oxidative stress and glucose depletion. In conclusion, osmotic and oxidative stress open Ca 2+ -permeable cation channels in erythrocytes, thus increasing cytosolic Ca 2+ activity and triggering erythrocyte apoptosis.

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“…51,52 The subsequent erythrocyte 'apoptosis' may then contribute to the derangement of microcirculation. Beyond that any erythrocyte disorder facilitating erythrocyte shrinkage, such as sickle cell disease, 28,53 thalassemia 54 or iron deficiency 55 could, to the extent as it leads to activation of the cell volume regulatory cation channels, trigger premature 'apoptosis' and thus accelerate erythrocyte death. 56 Erythrocyte phosphatidylserine exposure may not only be regulated by PGE 2 formed by stressed erythrocytes but also may be triggered by PGE 2 from other sources.…”

Section: -43mentioning

confidence: 99%

PGE2 in the regulation of programmed erythrocyte death

et al. 2005

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Hyperosmotic shock, energy depletion, or removal of extracellular Cl À activates Ca 2 þ -permeable cation channels in erythrocyte membranes. Subsequent Ca 2 þ 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 À removal triggered the release of prostaglandin E 2 (PGE 2 ). In whole-cell recording, activation of the cation channels by Cl À 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 À removal. PGE 2 (but not thromboxane) induced cation channel activation, increase in cytosolic Ca 2 þ 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 À removal stimulates erythrocyte PS exposure through PGE 2 formation and subsequent activation of Ca 2+ -permeable cation channels.

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Prevalence of hypochromia (without microcytosis) vs microcytosis (without hypochromia) in iron deficiency

Abstract: The usefulness of hypochromia (MCH or =… Show more

Cited by 45 publications

References 7 publications

Stimulation of erythrocyte ceramide formation by platelet-activating factor

Stimulation of erythrocyte ceramide formation by platelet-activating factor

Cation channels trigger apoptotic death of erythrocytes

PGE2 in the regulation of programmed erythrocyte death

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