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Blood, Vol. 95 No. 2 (January 15), 2000:
pp. 528-534
The residual megakaryocyte and platelet production in
c-Mpl-deficient mice is not dependent on the actions of
interleukin-6, interleukin-11, or leukemia inhibitory factor
Timothy Gainsford,
Harshal Nandurkar,
Donald Metcalf,
Lorraine Robb,
C. Glenn Begley, and
Warren S. Alexander
From The Walter and Eliza Hall Institute for Medical Research, the
Cooperative Research Centre for Cellular Growth Factors and the Rotary
Bone Marrow Research Laboratories, Royal Melbourne Hospital, Victoria,
Australia.
Mice lacking thrombopoietin (TPO) or its receptor c-Mpl are severely
thrombocytopenic, consistent with a dominant physiological role for
this cytokine in megakaryocytopoiesis. However, these mice remain
healthy and show no signs of spontaneous hemorrhage, implying that
TPO-independent mechanisms for platelet production exist and are
sufficient for hemostasis. To investigate the roles of cytokines that
act through the gp130 signaling chain in the residual platelet
production of mpl -/- mice, mpl
-/-IL-6-/-,
mpl-/-LIF-/-, and
mpl-/-IL-11R -/-
double-mutant mice were generated. In each of these compound mutants,
the number of circulating platelets was no lower than that observed in
mice lacking only the c-mpl gene. Moreover, the deficits in the
numbers of megakaryocytes and megakaryocyte progenitor cells in the
bone marrow and spleen were no further exacerbated in
mpl-/-IL-6-/-,
mpl-/-LIF-/-, or
mpl-/-IL-11R-/-
double-mutant mice compared with those in Mpl-deficient animals. In
single IL-6-/-, LIF-/-, and
IL-11R-/- mutant mice, platelet production was
normal. These data establish that, as single regulators, IL-6, IL-11,
and LIF have no essential role in normal steady-state
megakaryocytopoiesis, and are not required for the residual
megakaryocyte and platelet production seen in the
c-mpl-/- mouse.
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