On the kinetics of erythroid cell differentiation in fetal mice. I. Microspectrophotometric determination of the hemoglobin content in erythroid cells during gestation

1973 ◽  
Vol 81 (3) ◽  
pp. 323-337 ◽  
Author(s):  
Rudolf Steiner ◽  
Helmut Vogel
Keyword(s):  
Cell Differentiation ◽  
Erythroid Cell ◽  
Erythroid Cells ◽  
Hemoglobin Content ◽  
Fetal Mice ◽  
Erythroid Cell Differentiation ◽  
Kinetics Of ◽  
In Erythroid Cells

scholarly journals AKT induces erythroid-cell maturation of JAK2-deficient fetal liver progenitor cells and is required for Epo regulation of erythroid-cell differentiation

Blood ◽  
2006 ◽  
Vol 107 (5) ◽  
pp. 1888-1891 ◽  
Author(s):  
Saghi Ghaffari ◽  
Claire Kitidis ◽  
Wei Zhao ◽  
Dragan Marinkovic ◽  
Mark D. Fleming ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Cell Survival ◽  
Fetal Liver ◽  
Dominant Negative ◽  
Cell Maturation ◽  
Erythroid Cell ◽  
Erythroid Cells ◽  
Serine Threonine Kinase ◽  
Regulation Of Expression ◽  
Erythroid Cell Differentiation

AKT serine threonine kinase of the protein kinase B (PKB) family plays essential roles in cell survival, growth, metabolism, and differentiation. In the erythroid system, AKT is known to be rapidly phosphorylated and activated in response to erythropoietin (Epo) engagement of Epo receptor (EpoR) and to sustain survival signals in cultured erythroid cells. Here we demonstrate that activated AKT complements EpoR signaling and supports erythroid-cell differentiation in wild-type and JAK2-deficient fetal liver cells. We show that erythroid maturation of AKT-transduced cells is not solely dependent on AKT-induced cell survival or proliferation signals, suggesting that AKT transduces also a differentiation-specific signal downstream of EpoR in erythroid cells. Down-regulation of expression of AKT kinase by RNA interference, or AKT activity by expression of dominant negative forms, inhibits significantly fetal liver–derived erythroid-cell colony formation and gene expression, demonstrating that AKT is required for Epo regulation of erythroid-cell maturation.

scholarly journals Decreased differentiation of erythroid cells exacerbates ineffective erythropoiesis in β-thalassemia

Blood ◽  
2008 ◽  
Vol 112 (3) ◽  
pp. 875-885 ◽  
Author(s):  
Ilaria V. Libani ◽  
Ella C. Guy ◽  
Luca Melchiori ◽  
Raffaella Schiro ◽  
Pedro Ramos ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
S Phase ◽  
Erythroid Cell ◽  
Erythroid Cells ◽  
Ineffective Erythropoiesis ◽  
Ki 67 ◽  
Jak2 Inhibitor ◽  
Normal Percentage ◽  
Erythroid Cell Differentiation

Abstract In β-thalassemia, the mechanism driving ineffective erythropoiesis (IE) is insufficiently understood. We analyzed mice affected by β-thalassemia and observed, unexpectedly, a relatively small increase in apoptosis of their erythroid cells compared with healthy mice. Therefore, we sought to determine whether IE could also be characterized by limited erythroid cell differentiation. In thalassemic mice, we observed that a greater than normal percentage of erythroid cells was in S-phase, exhibiting an erythroblast-like morphology. Thalassemic cells were associated with expression of cell cycle–promoting genes such as EpoR, Jak2, Cyclin-A, Cdk2, and Ki-67 and the antiapoptotic protein Bcl-XL. The cells also differentiated less than normal erythroid ones in vitro. To investigate whether Jak2 could be responsible for the limited cell differentiation, we administered a Jak2 inhibitor, TG101209, to healthy and thalassemic mice. Exposure to TG101209 dramatically decreased the spleen size but also affected anemia. Although our data do not exclude a role for apoptosis in IE, we propose that expansion of the erythroid pool followed by limited cell differentiation exacerbates IE in thalassemia. In addition, these results suggest that use of Jak2 inhibitors has the potential to profoundly change the management of this disorder.

scholarly journals ERYTHROID CELL DIFFERENTIATION AND THE INHIBITION OF CYTOKINESIS BY CYTOCHALASIN

1971 ◽  
Vol 51 (2) ◽  
pp. 433-439 ◽  
Author(s):  
Linda W. Reynolds ◽  
Vernon M. Ingram
Keyword(s):  
Cell Differentiation ◽  
Cytochalasin B ◽  
Erythroid Cell ◽  
Tissue Cultures ◽  
Erythroid Cells ◽  
Young Chick ◽  
Erythroid Cell Differentiation

Cytochalasin B produces multinucleated erythroid cells in tissue cultures of very young chick blastoderms. There is no apparent qualitative interference with differentiation and maturation of erythroid cells, but the amounts produced are reduced 4- and 10-fold. These effects of cytochalasin are readily reversible.

scholarly journals Changes in globin messenger RNA content during erythroid cell differentiation.

1975 ◽  
Vol 250 (15) ◽  
pp. 6054-6058
Author(s):  
F Ramirez ◽  
R Gambino ◽  
G M Maniatis ◽  
R A Rifkind ◽  
P A Marks ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Messenger Rna ◽  
Erythroid Cell ◽  
Rna Content ◽  
Erythroid Cell Differentiation

Suppression of erythroid cell differentiation in mouse embryos exposed to retinoic acid in utero

1989 ◽  
Vol 223 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Yoshiko Yasuda ◽  
Hiroyoshi Konishi ◽  
Takuya Matsuo ◽  
Takashi Tanimura
Keyword(s):  
Retinoic Acid ◽  
Cell Differentiation ◽  
In Utero ◽  
Mouse Embryos ◽  
Erythroid Cell ◽  
Erythroid Cell Differentiation

scholarly journals Antagonistic Regulation of β-Globin Gene Expression by Helix-Loop-Helix Proteins USF and TFII-I

2006 ◽  
Vol 26 (18) ◽  
pp. 6832-6843 ◽  
Author(s):  
Valerie J. Crusselle-Davis ◽  
Karen F. Vieira ◽  
Zhuo Zhou ◽  
Archana Anantharaman ◽  
Jörg Bungert
Keyword(s):  
Gene Expression ◽  
Rna Polymerase Ii ◽  
Control Region ◽  
Adult Stage ◽  
Globin Gene ◽  
Locus Control Region ◽  
Erythroid Cell ◽  
Erythroid Cells ◽  
Globin Gene Expression ◽  
In Erythroid Cells

ABSTRACT The human β-globin genes are expressed in a developmental stage-specific manner in erythroid cells. Gene-proximal cis-regulatory DNA elements and interacting proteins restrict the expression of the genes to the embryonic, fetal, or adult stage of erythropoiesis. In addition, the relative order of the genes with respect to the locus control region contributes to the temporal regulation of the genes. We have previously shown that transcription factors TFII-I and USF interact with the β-globin promoter in erythroid cells. Herein we demonstrate that reducing the activity of USF decreased β-globin gene expression, while diminishing TFII-I activity increased β-globin gene expression in erythroid cell lines. Furthermore, a reduction of USF activity resulted in a significant decrease in acetylated H3, RNA polymerase II, and cofactor recruitment to the locus control region and to the adult β-globin gene. The data suggest that TFII-I and USF regulate chromatin structure accessibility and recruitment of transcription complexes in the β-globin gene locus and play important roles in restricting β-globin gene expression to the adult stage of erythropoiesis.

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