scholarly journals The embryonic origins of erythropoiesis in mammals

Blood ◽  
2012 ◽  
Vol 119 (21) ◽  
pp. 4828-4837 ◽  
Author(s):  
Margaret H. Baron ◽  
Joan Isern ◽  
Stuart T. Fraser
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Postnatal Life ◽  
Fetal Life ◽  
Cell Type ◽  
Mammalian Embryo ◽  
Cell Lineages ◽  
The Past ◽  
Distinguishing Features

Abstract Erythroid (red blood) cells are the first cell type to be specified in the postimplantation mammalian embryo and serve highly specialized, essential functions throughout gestation and postnatal life. The existence of 2 developmentally and morphologically distinct erythroid lineages, primitive (embryonic) and definitive (adult), was described for the mammalian embryo more than a century ago. Cells of the primitive erythroid lineage support the transition from rapidly growing embryo to fetus, whereas definitive erythrocytes function during the transition from fetal life to birth and continue to be crucial for a variety of normal physiologic processes. Over the past few years, it has become apparent that the ontogeny and maturation of these lineages are more complex than previously appreciated. In this review, we highlight some common and distinguishing features of the red blood cell lineages and summarize advances in our understanding of how these cells develop and differentiate throughout mammalian ontogeny.

Pathophysiology of Thrombocytopenia and Anemia in Mice Lacking Transcription Factor NF-E2

Blood ◽  
1999 ◽  
Vol 94 (9) ◽  
pp. 3037-3047 ◽  
Author(s):  
Jack Levin ◽  
Jin-Peng Peng ◽  
Georgiann R. Baker ◽  
Jean-Luc Villeval ◽  
Patrick Lecine ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Fetal Life ◽  
Wild Type ◽  
Cell Lineages ◽  
Cell Fragments ◽  
Proliferation Potential

Abstract Expression of the p45 subunit of transcription factor NF-E2 is restricted to selected blood cell lineages, including megakaryocytes and developing erythrocytes. Mice lacking p45 NF-E2 show profound thrombocytopenia, resulting from a late arrest in megakaryocyte differentiation, and a number of red blood cell defects, including anisocytosis and hypochromia. Here we report results of studies aimed to explore the pathophysiology of these abnormalities. Mice lacking NF-E2 produce very few platelet-like particles that display highly disorganized ultrastructure and respond poorly to platelet agonists, features consistent with the usually lethal hemorrhage in these animals. Thrombocytopenia was evident during fetal life and was not corrected by splenectomy in adults. Surprisingly, fetal NF-E2–deficient megakaryocyte progenitors showed reduced proliferation potential in vitro. Thus, NF-E2 is required for regulated megakaryocyte growth as well as for differentiation into platelets. All the erythroid abnormalities were reproduced in lethally irradiated wild-type recipients of hematopoietic cells derived from NF-E2-null fetuses. Whole blood from mice lacking p45 NF-E2 showed numerous small red blood cell fragments; however, survival of intact erythrocytes in vivo was indistinguishable from control mice. Considered together, these observations indicate a requirement for NF-E2 in generating normal erythrocytes. Despite impressive splenomegaly at baseline, mice lacking p45 NF-E2 survived splenectomy, which resulted in increased reticulocyte numbers. This reveals considerable erythroid reserve within extra-splenic sites of hematopoiesis and suggests a role for the spleen in clearing abnormal erythrocytes. Our findings address distinct aspects of the requirements for NF-E2 in blood cell homeostasis and establish its roles in proper differentiation of megakaryocytes and erythrocytes.

Pathophysiology of Thrombocytopenia and Anemia in Mice Lacking Transcription Factor NF-E2

Blood ◽  
1999 ◽  
Vol 94 (9) ◽  
pp. 3037-3047 ◽  
Author(s):  
Jack Levin ◽  
Jin-Peng Peng ◽  
Georgiann R. Baker ◽  
Jean-Luc Villeval ◽  
Patrick Lecine ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Fetal Life ◽  
Wild Type ◽  
Cell Lineages ◽  
Cell Fragments ◽  
Proliferation Potential

Expression of the p45 subunit of transcription factor NF-E2 is restricted to selected blood cell lineages, including megakaryocytes and developing erythrocytes. Mice lacking p45 NF-E2 show profound thrombocytopenia, resulting from a late arrest in megakaryocyte differentiation, and a number of red blood cell defects, including anisocytosis and hypochromia. Here we report results of studies aimed to explore the pathophysiology of these abnormalities. Mice lacking NF-E2 produce very few platelet-like particles that display highly disorganized ultrastructure and respond poorly to platelet agonists, features consistent with the usually lethal hemorrhage in these animals. Thrombocytopenia was evident during fetal life and was not corrected by splenectomy in adults. Surprisingly, fetal NF-E2–deficient megakaryocyte progenitors showed reduced proliferation potential in vitro. Thus, NF-E2 is required for regulated megakaryocyte growth as well as for differentiation into platelets. All the erythroid abnormalities were reproduced in lethally irradiated wild-type recipients of hematopoietic cells derived from NF-E2-null fetuses. Whole blood from mice lacking p45 NF-E2 showed numerous small red blood cell fragments; however, survival of intact erythrocytes in vivo was indistinguishable from control mice. Considered together, these observations indicate a requirement for NF-E2 in generating normal erythrocytes. Despite impressive splenomegaly at baseline, mice lacking p45 NF-E2 survived splenectomy, which resulted in increased reticulocyte numbers. This reveals considerable erythroid reserve within extra-splenic sites of hematopoiesis and suggests a role for the spleen in clearing abnormal erythrocytes. Our findings address distinct aspects of the requirements for NF-E2 in blood cell homeostasis and establish its roles in proper differentiation of megakaryocytes and erythrocytes.

Real-time Red Blood Cell Counting and Osmolarity Analysis using a Photoacoustic-based Microfluidic System

Lab on a Chip ◽  
2021 ◽  
Author(s):  
Wenxiu Zhao ◽  
Haibo Yu ◽  
Yangdong Wen ◽  
Hao Luo ◽  
Boliang Jia ◽  
...  
Keyword(s):  
Blood Cell ◽  
Physical Properties ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Diagnostic Procedure ◽  
Microfluidic System ◽  
Cell Counting ◽  
Blood Samples ◽  
System P ◽  
Blood Cell Counting

Counting the number of red blood cells (RBCs) in blood samples is a common clinical diagnostic procedure, but conventional methods are unable to provide the size and other physical properties...

Microfluidic electrical impedance assessment of red blood cell mediated microvascular occlusion

Lab on a Chip ◽  
2021 ◽  
Author(s):  
Yuncheng Man ◽  
Debnath Maji ◽  
Ran An ◽  
Sanjay Ahuja ◽  
Jane A Little ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Blood Cell ◽  
Red Blood Cells ◽  
Sickle Cell ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Electrical Impedance ◽  
Cell Disease ◽  
Blood Disorders

Alterations in the deformability of red blood cells (RBCs), occurring in hemolytic blood disorders such as sickle cell disease (SCD), contributes to vaso-occlusion and disease pathophysiology. However, there are few...

Red blood cell as glucose carrier: significance for placental and cerebral glucose transfer

1984 ◽  
Vol 246 (3) ◽  
pp. R289-R298 ◽  
Author(s):  
J. A. Jacquez
Keyword(s):  
Blood Cell ◽  
Glucose Transport ◽  
Blood Brain Barrier ◽  
Red Blood Cell ◽  
High Capacity ◽  
Brain Barrier ◽  
Fetal Life ◽  
Red Cell Membrane ◽  
Glucose Transfer ◽  
Blood Brain

At plasma glucose values of 5 mM (90 mg/100 ml) the maximum glucose transport capacity of the human red cell membrane is 12,000 times the rate of glucose utilization by the red blood cell. Mammals, other than primates, that have been tested have a comparable high-capacity system during fetal life, which is lost soon after birth. It has been suggested that the availability of the water space of the red blood cell for distribution of glucose facilitates transfer across the placenta during fetal life in all mammals and across the blood-brain barrier in adult primates. Though plausible, more comparative studies of glucose transport in red blood cells of other species and direct experimental evaluations of the contribution of the red blood cell to glucose transfer across the placenta and the blood-brain barrier are needed.

Reorientation of a single red blood cell during sedimentation

2016 ◽  
Vol 806 ◽  
pp. 102-128 ◽  
Author(s):  
D. Matsunaga ◽  
Y. Imai ◽  
C. Wagner ◽  
T. Ishikawa
Keyword(s):  
Angular Velocity ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Driving Force ◽  
Viscosity Ratio ◽  
Orientation Angle ◽  
Bond Number ◽  
Vertical Orientation ◽  
Main Factors

The reorientation phenomenon of a single red blood cell during sedimentation is simulated using the boundary element method. The cell settles downwards due to a density difference between the internal and external fluids, and it changes orientation toward a vertical orientation regardless of Bond number or viscosity ratio. The reorientation phenomenon is explained by a shape asymmetry caused by the gravitational driving force, and the shape asymmetry increases almost linearly with the Bond number. When velocities are normalised by the driving force, settling/drifting velocities are weak functions of the Bond number and the viscosity ratio, while the angular velocity of the reorientation drastically changes with these parameters: the angular velocity is smaller for lower Bond number or higher viscosity ratio. As a consequence, trajectories of the sedimentation are also affected by the angular velocity, and blood cells with slower reorientation travel longer distances in the drifting direction. We also explain the mechanism of the reorientation using an asymmetric dumbbell. From the analysis, we show that the magnitude of the angular velocity is explained by two main factors: the shape asymmetry and the instantaneous orientation angle.

Permeation of the luminal capillary glycocalyx is determined by hyaluronan

1999 ◽  
Vol 277 (2) ◽  
pp. H508-H514 ◽  
Author(s):  
Charmaine B. S. Henry ◽  
Brian R. Duling
Keyword(s):  
Blood Cell ◽  
Red Blood Cells ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Enzyme Treatment ◽  
Apical Surface ◽  
Bright Field ◽  
Endothelial Surface ◽  
The Difference

The endothelial cell glycocalyx influences blood flow and presents a selective barrier to movement of macromolecules from plasma to the endothelial surface. In the hamster cremaster microcirculation, FITC-labeled Dextran 70 and larger molecules are excluded from a region extending almost 0.5 μm from the endothelial surface into the lumen. Red blood cells under normal flow conditions are excluded from a region extending even farther into the lumen. Examination of cultured endothelial cells has shown that the glycocalyx contains hyaluronan, a glycosaminoglycan which is known to create matrices with molecular sieving properties. To test the hypothesis that hyaluronan might be involved in establishing the permeation properties of the apical surface glycocalyx in vivo, hamster microvessels in the cremaster muscle were visualized using video microscopy. After infusion of one of several FITC-dextrans (70, 145, 580, and 2,000 kDa) via a femoral cannula, microvessels were observed with bright-field and fluorescence microscopy to obtain estimates of the anatomic diameters and the widths of fluorescent dextran columns and of red blood cell columns (means ± SE). The widths of the red blood cell and dextran exclusion zones were calculated as one-half the difference between the bright-field anatomic diameter and the width of the red blood cell column or dextran column. After 1 h of treatment with active Streptomyces hyaluronidase, there was a significant increase in access of 70- and 145-kDa FITC-dextrans to the space bounded by the apical glycocalyx, but no increase in access of the red blood cells or in the anatomic diameter in capillaries, arterioles, and venules. Hyaluronidase had no effect on access of FITC-Dextrans 580 and 2,000. Infusion of a mixture of hyaluronan and chondroitin sulfate after enzyme treatment reconstituted the glycocalyx, although treatment with either molecule separately had no effect. These results suggest that cell surface hyaluronan plays a role in regulating or establishing permeation of the apical glycocalyx to macromolecules. This finding and our prior observations suggest that hyaluronan and other glycoconjugates are required for assembly of the matrix on the endothelial surface. We hypothesize that hyaluronidase creates a more open matrix, enabling smaller dextran molecules to penetrate deeper into the glycocalyx.

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