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Blood, 15 November 2002, Vol. 100, No. 10, pp. 3812-3818
RED CELLS
Phenotypes and phosphatidylinositol glycan-class A gene
abnormalities during cell differentiation and maturation from precursor
cells to mature granulocytes in patients with paroxysmal nocturnal
hemoglobinuria
Tatsuyuki Kai,
Tsutomu Shichishima,
Hideyoshi Noji,
Tetsuo Yamamoto,
Masatoshi Okamoto,
Kazuhiko Ikeda, and
Yukio Maruyama
From the First Department of Internal Medicine,
Fukushima Medical University, Fukushima, Japan, and the Third
Department of Internal Medicine, National Defense Medical College,
Saitama, Japan.
To define the phosphatidylinositol glycan-class A (PIG-A)
gene abnormality in precursor cells and the changes of expression of
glycosylphosphatidylinositol-anchored protein and contribution of
paroxysmal nocturnal hemoglobinuria (PNH) clones with PIG-A gene
abnormalities among various cell lineages during differentiation and
maturation, we investigated CD59 expression on bone marrow CD34+ cells and peripheral granulocytes from 3 patients
with PNH and the PIG-A gene abnormalities in the CD59 ,
CD59+/, and CD59+ populations by nucleotide
sequence analyses. We also performed clonogeneic assays of
CD34+CD59+ and
CD34+CD59 cells from 2 of the patients and
examined the PIG-A gene abnormalities in the cultured cells. In case 1, the CD34+ cells and granulocytes consisted of
CD59 and CD59+ populations and
CD59, CD59+/, and CD59+
populations, respectively. Sequence analyses indicated that mutation 1-2 was in the CD59+/ granulocyte population (20 of 20)
and the CD34+CD59 population (2 of 38). In
cases 2 and 3, the CD34+ cells and granulocytes consisted
of CD59+ and CD59 cells. Sequence analyses in
case 3 showed that mutation 3-2 was not in
CD34+CD59 cells and was present in the
CD59 granulocyte population. However, PIG-A gene analysis
of cultured CD34+CD59 cells showed that they
had the mutation. This analysis also revealed that there were some
other mutations, which were not found in CD34+CD59 cells and CD59 or
CD59+/ granulocytes in vivo, and that sometimes they were
distributed specifically among different cell lineages. In conclusion,
our findings suggest that PNH clones might contribute qualitatively and
quantitatively differentially to specific blood cell lineages during
differentiation and maturation of hematopoietic stem cells.
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