title: Defect of erythropoiesis in non-leukaemic AKR mice.
abstract: The kinetics of the CFU population and of erythropoiesis were investigated in the AKR strain mouse prior to the onset of thymic leukaemias: haemopoiesis was compared in syngeneic AKR, semi-allogenic C3H and (C3H X AKR) F1 mice injected with AKR stem cells. These experiments demonstrate that the reduction in The number of spleen colonies previously described by Perkins et al. (1971) in syngeneic hosts, as compared to semi-allogenic C3H hosts, is actually related to defective erythropoiesis resulting from a dysfunction of the AKR haemopoietic inductive microenvironment (HIM). Erythropoietin secretion is normal in AKR mice. The early haemopoietic events related to the stem cell: lodgement of the CFU ('f' factor) and doubling time, are not disturbed, but the onset of CFU proliferation is markedly delayed in the AKR strain. The main expression of the AKR HIM dysfunction is a significant reduction in the number of erythroid (E) colonies and an impaired output of red blood cells per E-colony in the syngeneic host as compared to the allogenic one. In addition, data indicate that a weakly histo-incompatible system, such as that in C3H and hybrid hosts, does not interfere with the stages of haemopoiesis except by lengthening the doubling time of the CFU. The results, on the whole, emphasize the prevalent influence of HIM.
mesh_terms: D000818:Animals; D001853:Bone Marrow / Q000502:physiology; D002455:Cell Division; D004920:Erythropoiesis; D004921:Erythropoietin / Q000097:blood / Q000494:pharmacology; D005260:Female; D006400:Hematocrit; D006412:Hematopoietic Stem Cells / Q000166:cytology*; D006470:Hemorrhage; D007700:Kinetics; D008297:Male; D051379:Mice; D008806:Mice, Inbred AKR; D008809:Mice, Inbred C3H
chemical_list: D004921:Erythropoietin