SOME OBSERVATIONS OF HEMATOPOIETIC STATUS INVIVO AND INVITRO ON MICE OF GENOTYPE S1-S1D

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  • 1 January 1976
    • journal article
    • research article
    • Vol. 48  (4) , 601-608
Abstract
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, the formation of surface associated fibroblastic plaques that could stimulate hematopoietic colony growth was observed, in addition to classical hematopoietic colonies. These plaques were hypothesized to be derived from bone marrow stroma precursors. Relative to controls, bone marrow derived from S1/S1d mice exhibited a significant decrease in hematopoietic colony-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.

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