Some observations of the hematopoietic status in vivo and in vitro on mice
of genotype S1/S1d
FD Wilson and L O'Grady
Studies on the mechanism of anemia in mice of genotype S1/S1d have
implicated the hematopoietic stroma (the hematopoietic inductive
microenvironment, HIM) rather than hematopoietic stem cells as the site of
the defect. Using methylcellulose-supported bone marrow culture systems, we
have observed, in addition to classical hematopoietic colonies, the
formation of surface associated fibroblastic plaques that could stimulate
hematopoietic colony growth. These plaques were hypothesized to be derived
from bone marrow stroma precursors. In view of the reported stromal-based
defect in S1/S1d mice, studies were initiated, using our culture system, to
determine if abnormalities exist in the plaque-forming potentials of these
mice. Relative to controls, bone marrow derived from S1/S1d mice exhibited
a significant decrease in hematopoietic colonly-forming units in culture,
but no differences were apparent in the absolute numbers of fibroblastic
plaque-forming units or in the ability of such plaques once derived to
stimulate hematopoietic colony growth when overlain with fresh normal bone
marrow preparations. Quantitative studies on the bone marrow of the S1/S1d
mice revealed a marked reduction in total nucleated cells per femur. The
importance of evaluating the results of bone marrow cultures in an absolute
(i.e., number of units per femur) rather than a relative (i.e., number of
units forming in a constant cell inoculum) term was underlined by these
studies.
Volume 48,
Issue 4,
pp. 601-608,
10/01/1976
Copyright © 1976 by The American Society of Hematology
