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Failure of stem cell factor to ameliorate AZT‐induced anemia in immunodeficient mice
Author(s) -
Hamburger Anne W.,
Zsebo Krisztina,
Chow FungPhing Rose
Publication year - 1993
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1993.tb00087.x
Subject(s) - stem cell factor , bone marrow , haematopoiesis , progenitor cell , reticulocyte , stem cell , anemia , erythropoiesis , zidovudine , immunology , medicine , endocrinology , biology , virus , viral disease , biochemistry , messenger rna , gene , genetics
Recent attempts to reduce 3′azido‐3′deoxythymidine (AZT)‐induced anemia in AIDS patients have focused both on AZT dose reduction and on the use of recombinant cytokines. The newly cloned cytokine stem cell factor (SCF) is a potent regulator of hematopoietic progenitor cell proliferation. Therefore, we attempted to ameliorate AZT‐induced anemia using stem cell factor (SCF) in the LP‐BM5 murine leukemia virus‐induced model of AIDS (MAIDS). SCF was administered with oral AZT for up to 1 month, and effects on erythropoiesis examined. SCF alone increased both splenic BFU‐E and CFU‐E. AZT alone also increased the number of splenic BFU‐E and CFU‐E. SCF, administered to AZT‐treated MAIDS mice, did not further enhance these increases. SCF increased bone marrow cellularity in AZT‐treated MAIDS mice. However, the total number of bone marrow BFU‐E was unaffected. In contrast, AZT, SCF, and the combination significantly decreased bone marrow CFU‐E. SCF alone increased the absolute numbers of peripheral blood reticulocytes in MAIDS mice, but did not increase reticulocyte numbers in AZT‐treated mice. SCF did not significantly increase hematocrits in either control or AZT‐treated mice. Further studies are needed to maximize the differentiating capacity of the enlarged erythroid progenitor cell pool induced by SCF.

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