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by upregulating and maintaining SMAD7. Consequently, RINF loss of expression will sensitize human erythroid progenitors to autocrine/paracrine TGFb-induced growth inhibition as a mechanism to prevent expansion of the erythroid pool. Our data also suggest that this signaling would be at least partly mediated through SMAD2 acti- vation and phosphorylation (Figure 4C), in agreement with a previous report on human bone marrow.35 The in
vivo relevance of these findings is strengthened by the cor- related RINF and SMAD7 mRNA expression in human bone marrow CD34+ cells. This correlation was also observed in MDS patients with del(5q) or 5q- but not in other forms of MDS, in which SMAD7 was silenced in most of the patients’ samples, whatever the RINF expres- sion level. This extinction of SMAD7 in other MDS could be explained by various mechanisms such as miRNA21
AB
C
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Figure 7. Legend on following page.
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