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Publication : The cellular basis for the defect in haemopoiesis in flexed-tailed mice. III. Restriction of the defect to erythropoietic progenitors capable of transient colony formation in vivo.

First Author  Gregory CJ Year  1975
Journal  Br J Haematol Volume  30
Issue  4 Pages  401-10
PubMed ID  1201223 Mgi Jnum  J:5582
Mgi Id  MGI:54059 Doi  10.1111/j.1365-2141.1975.tb01854.x
Citation  Gregory CJ, et al. (1975) The cellular basis for the defect in haemopoiesis in flexed-tailed mice. III. Restriction of the defect to erythropoietic progenitors capable of transient colony formation in vivo. Br J Haematol 30(4):401-10
abstractText  Three assays for erythropoietic progenitor cells have been applied to mice of genotype f/f and to nearly congenic +/+ controls. When f/f mice were tested for their ability to generate transient endogenous erythroid spleen colonies 4-6 days after 800 rads and 10 units of erythropoietin, the numbers of such colonies detected were greatly reduced, although normal numbers of spleen colonies appeared at later times (9-12 days) postirradiation. In contrast, cells capable of erythropoietic colony formation in culture (CFU-E) were present within the normal range in both f/f spleen and marrow and their sensitivity to erythropoietin in culture was the same as that found previously for CFU-E in the marrow and spleen of +/+ mice. Transfusion-induced plethora reduced the number of CFU-E in marrow to a similar extent in both f/f and +/+ mice; likewise, subsequent administration of 10 units of erythropoietin induced a rapid return in the number of marrow CFU-E in both genotypes. In the spleen, CFU-E numbers were approximately three-fold lower in f/f mice in each group. These results support the view that the 5 day assay for transient endogenous spleen colonies detects cells (TE-CFU) that are different from both CFU-E and pluripotent stem cells (CFU-S), although possibly overlapping to some extent with the immediate progenitors of CFU-E. The results also indicate that the generation or maturation of TE-CFU represents a primary site of expression of the f/f defect.
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