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Blood, 15 August 2002, Vol. 100, No. 4, pp. 1123-1132
PLENARY PAPER
Development of myelofibrosis in mice genetically impaired for
GATA-1 expression (GATA-1low mice)
Alessandro Maria Vannucchi,
Lucia Bianchi,
Cristina Cellai,
Francesco Paoletti,
Rosa Alba Rana,
Rodolfo Lorenzini,
Giovanni Migliaccio, and
Anna Rita Migliaccio
From the Departments of Ematologia and
Oncologia-Patologia Sperimentale, University of Florence; Azienda
Ospedaliera Careggi, Florence; Department of Biomorfologia, University
G. D'Annunzio, Chieti; and Servizio Qualità Sicurezza Animale,
Biologia Cellulare, and Biochimica Clinica, Istituto Superiore
Sanità, Rome, Italy.
The phenotype induced by the GATA-1low (neo HS)
mutation is here further characterized by analyzing the hemopoietic
system during the aging (up to 20 months) of a GATA-1low
colony (135 mutants and 40 normal littermates). Mutants expressed normal hematocrit values (Hct = 45.9 ± 4.0) until 12 months but became anemic from 15 months on (Hct = 30.9 ± 3.9;
P < .05). Anemia was associated with several markers of
myelofibrosis such as the presence of tear-drop poikilocytes and
progenitor cells in the blood, collagen fibers in the marrow and in the
spleen, and hemopoietic foci in the liver. Semiquantitative reverse
transcription-polymerase chain reaction showed that growth factor
genes implicated in the development of myelofibrosis (such as
osteocalcin, transforming growth factor- 1, platelet-derived growth
factor, and vascular endothelial growth factor) were all expressed in
the marrow from the mutants at higher levels than in corresponding
normal tissues. The GATA-1low mutants experienced a slow
progression of the disease because the final exitus was not observed
until at least 15 months with a probability of survival more favorable
than that of W/Wv mice concurrently kept in the animal
facility (P < .001, by Kaplan-Meier analysis). In
conclusion, impaired GATA-1 expression may contribute to the
development of myelofibrosis, and the GATA-1low mutants may
represent a suitable animal model for the human disease that may shed
light on its pathogenesis.
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