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Hematopoietic repopulation of adult mice with beta-thalassemia
JE Barker and ST Compton
Jackson Laboratory, Bar Harbor, ME 04609.
Deletion of the murine beta-major globin gene on chromosome 7 causes a
severe, hypochromic anemia in homozygous mice. We show that over 50% of the
homozygous mice die either in utero or at birth. Mice heterozygous for the
deletion have a slightly increased percentage of reticulocytes when
compared with normal mice, but no clinical anemia. As a therapeutic
measure, we transplanted 2 x 10(6) congenic genetically marked normal (+/+)
marrow cells into adult homozygous and control heterozygous mice.
Pretreatment with marrow ablative irradiation was required to obtain
significant percentages of donor peripheral blood cells in the homozygous
mice. Red blood cell (RBC) counts normalized after pretransplantation
irradiation of thalassemic mice with nonlethal doses as low as 400 R. The
thalassemic mice irradiated with 200, 400, and 600 R were erythroid-cell
chimeras and remained so for at least 8 months posttransplantation, whereas
those irradiated with 800 R had primarily donor erythrocytes by 8 weeks.
RBC replacement preceded non- erythroid cell replacement at 200, 400, and
600 R. This selective repopulation was more noticeable in the thalassemic
mice than in control mice. The fact that chimeric mice are cured, coupled
with a recent observation by others that erythroid replacement occurs in
unirradiated newborn thalassemic mice, suggest transplantation therapy in
utero might augment survival.
Volume 83,
Issue 3,
pp. 828-832,
02/01/1994
Copyright © 1994 by The American Society of Hematology
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