Compensatory splenic hemopoiesis in beta-thalassemic mice.
beta-Thalassemic mice, homozygous for the deletion of the beta major-globin gene, were investigated for compensatory hemopoiesis in bone marrow and spleen. Apart from characteristic severe anemia, these mice have a marked granulocytosis, monocytosis and lymphocytosis. A large compensatory expansion of late (CFU-E) erythroid progenitor cells was demonstrated, predominantly in the spleen. Immature hemopoietic cells (CFU-S) were also expanded, as were early progenitor cells of erythroid (BFU-E), as well as granulocyte/macrophage (GM-CFU) and megakaryocytic (CFU-Meg) lineages. It is concluded that the persistent erythropoietic stress results in a selective expansion of immature hemopoietic cells and inappropriate production of nonerythroid blood cells from excess production of progenitor cells.
van den Bos
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C
Department of Radiobiology, Erasmus University, Rotterdam, The Netherlands.
Kieboom
D
D
Visser
T P
TP
Wagemaker
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G
D000818:Animals; D001853:Bone Marrow / Q000473:pathology / Q000502:physiology; D005260:Female; D006098:Granulocytes / Q000473:pathology / Q000502:physiology; D006410:Hematopoiesis / Q000502:physiology*; D006412:Hematopoietic Stem Cells / Q000473:pathology / Q000502:physiology; D008264:Macrophages / Q000473:pathology / Q000502:physiology; D008297:Male; D008533:Megakaryocytes / Q000473:pathology / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D013154:Spleen / Q000473:pathology / Q000503:physiopathology*; D017086:beta-Thalassemia / Q000473:pathology / Q000503:physiopathology*