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JE Barker and E McFarland
The alpha-thalassemic mouse has a hereditary microcytic anemia, almost
certainly has a shortened RBC life span, and is a potential candidate for
cell replacement therapy. In a routine study of bone marrow repopulating
capacity using hemoglobin as a cell marker, normal donor marrow cells, but
not alpha-thalassemic donor marrow cells, completely replaced the host
cells. Further analysis showed that at least 30 times more
alpha-thalassemic cells were required to outcompete normal donor cells
injected simultaneously. The results were more extreme then expected and
suggested a defect in a stem cell population as well as in the RBCs.
Evidence that the multipotent and erythroid-committed stem cells in
alpha-thalassemic mice are not decreased was shown by CFU-S and CFU-E
assays. The combined results indicate that the deletion expresses itself
most conspicuously in the RBC population. Tests were also performed to
analyze repopulation kinetics in the Hbath-J/+ mice. In unirradiated
alpha-thalassemic hosts, the hemoglobin from a normal donor persisted but
did not replace the host hemoglobin. Sublethally irradiated
alpha-thalassemic hosts, on the other hand, were easily repopulated with
normal cells. We conclude that the alpha-thalassemic mouse is a good model
for cell replacement therapy.
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| Copyright © 1985 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
