Static and dynamic rigidities of normal and sickle erythrocytes. Major influence of cell hemoglobin concentration.

Evans, Evan; Mohandas, Narla; Leung, A.Y.T.

doi:10.1172/jci111234

Cited by 198 publications

(128 citation statements)

References 21 publications

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“…The values for the bending modulus measured by micropipette-based studies are in the range of 50 kbT (10)(11)(12)(13)(14)(15)(16)(17)(18)(19) where kb is Boltzmann constant, and T is the temperature (Evans,1983). The bending modulus B of RBCs does not significantly change with temperature (Nash and Meiselman, 1985) or cell Hb concentration for both normal and sickle cells (Evans, Mohandas et al, 1984). The recent experiments (Betz, Lenz et al, 2009;Yoon, Hong et al, 2009) have also measured that the bending modulus of RBCs is of the order of 50 kbT.…”

Section: Shear Modulusmentioning

confidence: 90%

“…Shear modulus of lipid bilayers is essentially zero due to its fluidity nature; shear modulus of RBC is mainly contributed from the spectrin network. The shear moduli of RBC membranes have been extensively measured by micropipette aspiration; the values for µ are in the range of 6-10 µ N/m (Evans and La Celle,1975;Chien, Sung et al,1978;Waugh and Evans,1979;Evans, Mohandas et al,1984). Techniques based on optial tweezers (Lenormand, Hénon et al,2001;Dao, Lim et al,2003), magnetic twisting cytometry (Puig-de-Morales- Marinkovic, Turner et al, 2007), and dynamic membrane fluctuation measurements have also reported consistent values for µ.…”

Section: Shear Modulusmentioning

confidence: 96%

“…Using micropipette aspiration, the value for µ was measured as 91.7 µN/m (Evans, Mohandas et al,1984). Pt necessary to aspirate a whole RBC into the pipette.…”

Section: Micropipette Aspirationmentioning

confidence: 99%

“…Sickle RBCs have different morphologies depending on its density (Kaul, Fabry et al,1983;Evans, Mohandas et al,1984). After repeated sicklings, a fraction of RBCs becomes irreversibly sickled cells and they exhibit the most significant loss in deformability.…”

Section: Genetic Diseases: Sickle Cell Diseasementioning

confidence: 99%

See 3 more Smart Citations

Measurement Techniques for Red Blood Cell Deformability: Recent Advances

Kim¹,

K²,

Park³

2012

Blood Cell - An Overview of Studies in Hematology

109

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Section: Shear Modulusmentioning

confidence: 90%

Section: Shear Modulusmentioning

confidence: 96%

“…Using micropipette aspiration, the value for µ was measured as 91.7 µN/m (Evans, Mohandas et al,1984). Pt necessary to aspirate a whole RBC into the pipette.…”

Section: Micropipette Aspirationmentioning

confidence: 99%

Section: Genetic Diseases: Sickle Cell Diseasementioning

confidence: 99%

See 2 more Smart Citations

Measurement Techniques for Red Blood Cell Deformability: Recent Advances

Kim¹,

K²,

Park³

2012

Blood Cell - An Overview of Studies in Hematology

109

View full text Add to dashboard Cite

“…Sickle cells are consequently largely deoxygenated at the oxygen tension in the capillary circulation. Although sickle cell membrane abnormalities, abnormal cation homeostasis, and altered cation transport pathways have attracted much interest (Hebbel et al, 1980;Bookchin & Lew, 1980;Brugnara et al, 1989a;Joiner, 1993), it has become increasingly apparent that the decrease in deformability and filterability of sickle cells, as well as the formation of irreversible sickle cells, arises from intracellular polymerization of deoxy-HbSS (Evans et al, 1984;Green et al, 1988). The degree of polymerization of deoxy-HbSS, as well as the rate of polymer formation, is in turn highly dependent on oxygen tension, temperature and concentration of HbSS (Hofrichter et al, 1974;Noguchi et al, 1983).…”

mentioning

confidence: 99%

Do HbSS erythrocytes lose KCl in physiological conditions?

Dormandy¹,

Ellory²

1997

Br J Haematol

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Summary. KCl cotransporter activity in sickle (HbSS) red blood cells (RBCs) was measured in cells suspended in 'simple' physiological saline, saline augmented with inorganic salts, and autologous plasma. Our results showed that the transporter was only functioning at 20% of the level of cells in saline when cells were resuspended in autologous plasma. Kinetic analysis of the data showed that plasma decreased both V max and K m for K + of the transporter. The plasma factor(s) responsible was heat-stable and dialysable (i.e. size < 10 kD).Adding magnesium, calcium, inorganic phosphate or bicarbonate to 'simple' saline to mimic the effect of plasma revealed that Mg 2+ and Ca 2+ had no significant effect at physiological concentrations. P i was not effective at 1 . 1 mM , but did inhibit significantly (42Ϯ2%Þ at 5 . 6 mM . HCO ¹ 3 had a major inhibitory effect on K + influx when added to saline, and was identified as the principal candidate for the plasma effect.We suggest bicarbonate may play a significant role in modifying KCl cotransport, and hence HbSS cell volume in vivo. It acts by altering the set point of the transporter via the signalling systems involved in its regulation.

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The Gardos channel is responsible for CDNB-induced dense sickle cell formation

et al. 2000

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The red blood cells (RBCs) derived from blood taken from homozygous sickle cell (SS) patients demonstrate densities that are inversely proportional to the intracellular reduced glutathione (GSH) content. Addition of 1 mM 1-chloro-2,4-dinitrobenzene (CDNB) to low-density sickle cells (LDSS), at 4 degrees C, results in a shift of LDSS erythrocytes to high-density sickle cells (HDSS), with corresponding decreases in GSH. We have previously demonstrated that this CDNB effect was due to increased K(+) leakage and that dense cell formation could be inhibited by clotrimazole (specific for the Gardos channel) but not DIOA (specific for the K(+)-Cl(-) co-transport system) at pH 7.4 (Shartava et al. Am. J. Hematol. 1999;62:19-24). Here we demonstrate that clotrimazole (10 microM) inhibits dense cell formation at pH 7.1 and 6.8, while DIOA (1 mM) has no effect. As pH 6.8 is the optimal pH for the K(+)-Cl(-) co-transport system, we can now reasonably conclude that damage to the Gardos channel is responsible for CDNB-induced dense cell formation.

show abstract

Static and dynamic rigidities of normal and sickle erythrocytes. Major influence of cell hemoglobin concentration.

Cited by 198 publications

References 21 publications

Measurement Techniques for Red Blood Cell Deformability: Recent Advances

Measurement Techniques for Red Blood Cell Deformability: Recent Advances

Do HbSS erythrocytes lose KCl in physiological conditions?

The Gardos channel is responsible for CDNB-induced dense sickle cell formation

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