scholarly journals Mechanical Signature of Red Blood Cells Flowing Out of a Microfluidic Constriction Is Impacted by Membrane Elasticity, Cell Surface-to-Volume Ratio and Diseases

2020 ◽  
Vol 11 ◽  
Author(s):  
Magalie Faivre ◽  
Céline Renoux ◽  
Amel Bessaa ◽  
Lydie Da Costa ◽  
Philippe Joly ◽  
...  
1984 ◽  
Vol 74 (1) ◽  
pp. 173-180 ◽  
Author(s):  
Shoji Maruyama ◽  
Masahiko Sugiura ◽  
Michio Nakazawa ◽  
Hiroko Tomiyama ◽  
Miyuki Shizawa ◽  
...  

2018 ◽  
Vol 2 (20) ◽  
pp. 2581-2587 ◽  
Author(s):  
Innocent Safeukui ◽  
Pierre A. Buffet ◽  
Guillaume Deplaine ◽  
Sylvie Perrot ◽  
Valentine Brousse ◽  
...  

Abstract The current paradigm in the pathogenesis of several hemolytic red blood cell disorders is that reduced cellular deformability is a key determinant of splenic sequestration of affected red cells. Three distinct features regulate cellular deformability: membrane deformability, surface area-to-volume ratio (cell sphericity), and cytoplasmic viscosity. By perfusing normal human spleens ex vivo, we had previously showed that red cells with increased sphericity are rapidly sequestered by the spleen. Here, we assessed the retention kinetics of red cells with decreased membrane deformability but without marked shape changes. A controlled decrease in membrane deformability (increased membrane rigidity) was induced by treating normal red cells with increasing concentrations of diamide. Following perfusion, diamide-treated red blood cells (RBCs) were rapidly retained in the spleen with a mean clearance half-time of 5.9 minutes (range, 4.0-13.0). Splenic clearance correlated positively with increased membrane rigidity (r = 0.93; P < .0001). To determine to what extent this increased retention was related to mechanical blockade in the spleen, diamide-treated red cells were filtered through microsphere layers that mimic the mechanical sensing of red cells by the spleen. Diamide-treated red cells were retained in the microsphilters (median, 7.5%; range, 0%-38.6%), although to a lesser extent compared with the spleen (median, 44.1%; range, 7.3%-64.0%; P < .0001). Taken together, these results have implications for understanding the sensitivity of the human spleen to sequester red cells with altered cellular deformability due to various cellular alterations and for explaining clinical heterogeneity of RBC membrane disorders.


Blood ◽  
1959 ◽  
Vol 14 (4) ◽  
pp. 399-408 ◽  
Author(s):  
WILLIAM H. CROSBY

Abstract During all the stages of a red cell’s life the normal spleen exerts a normal function. Eight of these functions have been considered: (1) erythropoiesis; (2) an effect upon red cell production; (3) an effect upon maturation of the red cell surface; (4) the reservoir function; (5) the "culling function"; (6) iron turnover and storage; (7) the "pitting function"; (8) destruction of old red cells.


2014 ◽  
Vol 5 (9) ◽  
pp. 3463-3468 ◽  
Author(s):  
Ben Wang ◽  
Guangchuan Wang ◽  
Binjie Zhao ◽  
Jiajun Chen ◽  
Xueyun Zhang ◽  
...  

A strategy of surface engineering by using polydopamine was developed to shelter antigens on red blood cells and prevent coagulation reactions.


1998 ◽  
Vol 141 (6) ◽  
pp. 1335-1347 ◽  
Author(s):  
Hui Qiao ◽  
Sandra L. Pelletier ◽  
Lucas Hoffman ◽  
Jill Hacker ◽  
R. Todd Armstrong ◽  
...  

We tested the role of the “spring-loaded” conformational change in the fusion mechanism of the influenza hemagglutinin (HA) by assessing the effects of 10 point mutants in the region of high coiled-coil propensity, HA2 54–81. The mutants included proline substitutions at HA2 55, 71, and 80, as well as a double proline substitution at residues 55 and 71. Mutants were expressed in COS or 293T cells and assayed for cell surface expression and structural features as well as for their ability to change conformation and induce fusion at low pH. We found the following: Specific mutations affected the precise carbohydrate structure and folding of the HA trimer. All of the mutants, however, formed trimers that could be expressed at the cell surface in a form that could be proteolytically cleaved from the precursor, HA0, to the fusion-permissive form, HA1-S-S-HA2. All mutants reacted with an antibody against the major antigenic site and bound red blood cells. Seven out of ten mutants displayed a wild-type (wt) or moderately elevated pH dependence for the conformational change. V55P displayed a substantial reduction (∼60– 80%) in the initial rate of lipid mixing. The other single mutants displayed efficient fusion with the same pH dependence as wt-HA. The double proline mutant V55P/ S71P displayed no fusion activity despite being well expressed at the cell surface as a proteolytically cleaved trimer that could bind red blood cells and change conformation at low pH. The impairment in fusion for both V55P and V55P/S71P was at the level of outer leaflet lipid mixing. We interpret our results in support of the hypothesis that the spring-loaded conformational change is required for fusion. An alternate model is discussed.


Author(s):  
Thibault J. Harmand ◽  
Novalia Pishesha ◽  
Fabian B. H. Rehm ◽  
Weiyi Ma ◽  
William B. Pinney ◽  
...  

2017 ◽  
Vol 42 (3) ◽  
pp. 1127-1138 ◽  
Author(s):  
Annarita Ciana ◽  
Cesare Achilli ◽  
Anjali Gaur ◽  
Giampaolo Minetti

Background/Aims: A high surface-to-volume ratio and a spectrin membrane-skeleton (MS) confer to the mammalian red blood cells (RBCs) their characteristic deformability, mechanical strength and structural stability. During their 120 days of circulatory life in humans, RBCs decrease in size, while remaining biconcave disks, owing to a coordinated decrease in membrane surface area and cell water. It is generally believed that part of the membrane is lost with the shedding of spectrin-free vesicles of the same type that can be obtained in vitro by different treatments. If this were true, an excess of MS would arise in old RBCs, with respect to the lipid bilayer. Aim of this paper was to investigate this aspect. Methods: Quantification of spectrin by electrophoretic methods was carried out in RBCs of different age. Results: Spectrin decreases, on a per cell basis, with RBC ageing. On the other hand, the membrane raft protein marker flotillin-2, while decreasing in the membrane of old cells, was found to be strongly depleted in the membrane of in vitro-induced vesicles. Conclusion: Part of the membrane-skeleton is probably lost together with part of the lipid bilayer in a balanced way. These findings point to a mechanism for the in vivo release of membrane that is different from that which is known to occur in vitro.


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