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- W2033740694 abstract "Abstract The tumor suppressor Smad4 mediates signaling by the transforming growth factor beta (TGF-β) superfamily of ligands. Previous studies showed that several TGF-β family members exert important functions in hematopoiesis. Here, we studied the role of Smad4 in adult murine hematopoiesis using the inducible Mx-Cre/loxP system. Mice with homozygous Smad4 deletion (Smad4Δ/Δ) developed severe anemia 6 to 8 weeks after induction (mean hemoglobin level 70 g/L). The anemia was not transplantable, as wild-type mice reconstituted with Smad4Δ/Δ bone marrow cells had normal peripheral blood counts. These mice did not develop an inflammatory disease typical for mice deficient in TGF-β receptors I and II, suggesting that the suppression of inflammation by TGF-β is Smad4 independent. The same results were obtained when Smad4 alleles were deleted selectively in hematopoietic cells using the VavCre transgenic mice. In contrast, lethally irradiated Smad4Δ/Δ mice that received wild-type bone marrow cells developed anemia similar to Smad4Δ/Δ mice that did not receive a transplant. Liver iron stores were decreased and blood was present in stool, indicating that the anemia was due to blood loss. Multiple polyps in stomach and colon represent a likely source of the bleeding. We conclude that Smad4 is not required for adult erythropoiesis and that anemia is solely the consequence of blood loss." @default.
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- W2033740694 date "2007-10-15" @default.
- W2033740694 modified "2023-09-29" @default.
- W2033740694 title "Normal erythropoiesis but severe polyposis and bleeding anemia in Smad4-deficient mice" @default.
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- W2033740694 doi "https://doi.org/10.1182/blood-2007-02-074393" @default.
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