Red Blood Cell Age, Pyruvate Kinase Activity, and Insulin Receptors: Evidence that Monocytes and RBCs May Behave Differently

Diabetes ◽  
1983 ◽  
Vol 32 (11) ◽  
pp. 1017-1022 ◽  
Author(s):  
A. Camagna ◽  
R. D. Pirro ◽  
L. Tardella ◽  
L. Rossetti ◽  
R. Lauro ◽  
...  
Diabetes ◽  
1983 ◽  
Vol 32 (11) ◽  
pp. 1017-1022 ◽  
Author(s):  
A. Camagna ◽  
R. De Pirro ◽  
L. Tardella ◽  
L. Rossetti ◽  
R. Lauro ◽  
...  

1984 ◽  
Vol 247 (5) ◽  
pp. E667-E674
Author(s):  
G. Baumann ◽  
J. G. MacCart

Insulin receptors are present in human erythrocytes and correlate negatively with cellular age. Little is known about the function of these receptors, about the precise kinetics of their decline during cell aging or about their fate after disappearance from the cells. To elucidate some of these questions, we have prepared red blood cell populations of widely varying cellular ages (ranging from the erythroblast stage to senescent mature erythrocytes) by isopycnic centrifugation on isosmolar density gradients. In addition, young red cells were cultured for 4 days in vitro to permit observation of short-term changes. In mature erythrocytes, insulin receptors decreased as an exponential function of cell age with an estimated half time of 40 days. A more rapid decline of insulin receptors occurred coincident with reticulocyte maturation. Loss of receptors from cultured cells was accompanied by appearance of a soluble insulin receptor in the medium. The effect of insulin on glucose utilization in erythroblast and reticulocyte preparations was negligible, as assessed by CO2 and lactate production. We conclude that 1) insulin receptors are progressively lost from the red blood cell after the erythroblast stage; 2) receptor loss is particularly rapid during reticulocyte maturation; 3) shedding of receptors into the extracellular environment is one reason for their depletion from cells; and 4) in basophilic erythroblasts and reticulocytes, insulin exhibits little metabolic action despite the relatively high receptor complement present in these cells.


1969 ◽  
Vol 7 (3) ◽  
pp. 253-254
Author(s):  
Robert S. Sparkes ◽  
Marjorie A. Baughan

2018 ◽  
Vol 42 (3) ◽  
pp. 151-157 ◽  
Author(s):  
Antony P McNamee ◽  
Kieran Richardson ◽  
Jarod Horobin ◽  
Lennart Kuck ◽  
Michael J Simmonds

Introduction: Accumulating evidence demonstrates that subhaemolytic mechanical stresses, typical of circulatory support, induce physical and biochemical changes to red blood cells. It remains unclear, however, whether cell age affects susceptibility to these mechanical forces. This study thus examined the sensitivity of density-fractionated red blood cells to sublethal mechanical stresses. Methods: Red blood cells were isolated and washed twice, with the least and most dense fractions being obtained following centrifugation (1500 g × 5 min). Red blood cell deformability was determined across an osmotic gradient and a range of shear stresses (0.3–50 Pa). Cell deformability was also quantified before and after 300 s exposure to shear stresses known to decrease (64 Pa) or increase (10 Pa) red blood cell deformability. The time course of accumulated sublethal damage that occurred during exposure to 64 Pa was also examined. Results: Dense red blood cells exhibited decreased capacity to deform when compared with less dense cells. Cellular response to mechanical stimuli was similar in trend for all red blood cells, independent of density; however, the magnitude of impairment in cell deformability was exacerbated in dense cells. Moreover, the rate of impairment in cellular deformability, induced by 64 Pa, was more rapid for dense cells. Relative improvement in red blood cell deformability, due to low-shear conditioning (10 Pa), was consistent for both cell populations. Conclusion: Red blood cell populations respond differently to mechanical stimuli: older (more dense) cells are highly susceptible to sublethal mechanical trauma, while cell age (density) does not appear to alter the magnitude of improved cell deformability following low-shear conditioning.


2004 ◽  
Vol 3 (3) ◽  
pp. 152-155 ◽  
Author(s):  
Hacer Yapicioglu ◽  
Mehmet Satar ◽  
Nejat Narli ◽  
Levent Kayrin ◽  
Ercan Tutak

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