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Studies on hematopoietic stem cells: XI. Lack of erythroid burst‐forming units (BFU‐E) in patients with aplastic anemia
Author(s) -
Moriyama Yoshiaki,
Sato Masatsugu,
Kinoshita Yasutami
Publication year - 1979
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830060103
Subject(s) - aplastic anemia , erythropoiesis , haematopoiesis , erythropoietin , immunology , anemia , in vitro , stem cell , biology , bone marrow , cfu gm , medicine , endocrinology , microbiology and biotechnology , biochemistry
The marrow concentration of erythropoietic precursors was examined in normal donors and patients with idiopathic aplastic anemia using a plasma clot culture system. On time course observations the heterogeneity of human erythroid precursors assayable in culture was demonstrated. To evaluate human erythropoiesis in vitro, the benzidine‐positive colonies were divided into three groups: small colony, containing 8–50 cells; medium‐sized colony, containing 50–500 cells; and large colony, containing more than 500 cells. The majority of the large colonies assumed the morphology of erythropoietic bursts (BFU‐E) consisted of several subcolonies. The small colonies were counted as CFU‐E1, the medium‐sized as CFU‐E2, and the large as BFU‐E to evaluate the erythroid precursor cell compartment in aplastic anemia. The marrow concentration of CFU‐E1 and CFU‐E2 was shown to be quantitatively diminished in aplastic anemia. In addition, there was no ability of the marrow cells from aplastic patients to grow BFU‐E in vitro even in the presence of a large dose of erythropoietin. This lack of BFU‐E colony growth may play an important role in the mechanism of the erythropoietic deficiency in aplastic anemia.