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Division of Experimental Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115
To assess the role of P-selectin and E-selectin in
megakaryocytopoiesis, in vitro assays were performed in animal
models deficient in both adhesion receptors. There was a significantly
greater number of IL-3-responsive megakaryocyte progenitors CFU
(CFU-MK) and an increase in immature megakaryoblasts in response to
IL-6 in the P-selectin-null mice compared with the wild-type controls.
Furthermore, P-selectin-null mice showed a greater number of CFU-MK
colonies derived from CD34+ cells in response to IL-3 or
IL-3 plus stem cell factor. A significant shift in baseline ploidy with
a reduction in 8N cells and an increase in 32N cells was also observed
in the P-selectin-null mice. Secretion of the inhibitory growth factor
TGF-
1 and not TGF-2 was significantly lower in the supernatants
of cultures containing bone marrow cells from P-selectin-deficient mice
as compared with those from the wild-type control bone marrow cells. No
differences in the responsiveness of murine CFU-MK, immature
megakaryocytes, or 5-fluorouracil-selected stem cells to
cytokines were observed in E-selectin-null mice as compared with the
control mice. These studies indicate that the absence of P-selectin,
and not E-selectin, resulted in an altered adhesion environment with
subsequent expansion of megakaryocyte progenitors and immature
megakaryoblasts, enhanced secretion of TGF-1, and apparent increased
responsiveness to inflammatory cytokines.
This article has been cited by other articles:
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  A. D. Blann, S. K. Nadar, and G. Y.H. Lip The adhesion molecule P-selectin and cardiovascular disease Eur. Heart J., December 2, 2003; 24(24): 2166 - 2179. [Abstract] [Full Text] [PDF]
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