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proliferation and differentiation, and leads to increased matrix mineralization (Yu et al., 2005; Yan et al, 2009). Our results show comparable level of gene expression of Axin2 in WT and nuli MSCs under basal conditions, as well as following Wnt3a stimulation. However, the expression of Lefl transcription factor, which mediates the nuclear response to Wnt signals, was diminished in Cd36-nuli MSCs before treatment, yet reached comparable levels to WT following Wnt3a stimulation, suggesting a similar response for both genotypes. The measure of Wnt signaling activity is needed to clarify the implication of canonical Wnt pathway in Cd36-nuli mice bonę metabolism. Activation of Lefl by P-catenin leads to transcription of numerous target genes involved in celi proliferation, including CcnD and c-myc (Westendorf et al., 2004). In light of this function, LeflKO mice are smaller than control littermates, display multiple defects in tissues formed from epithelial and mesenchymal progenitors and die shortly after birth (van Genderen et al., 1994). It has also been reported that Lefl haploinsufficiency generates a Iow bonę mass phenotype caused by reduced osteoblast function (Noh et al., 2009).

Combined, our findings suggest a significant contribution of CD36 to bonę homeostasis, both by directly influencing proliferation and apoptosis of marrow cells, and through systemie modulation of energy metabolism. MSCs lacking CD36 exhibit altered expression of genes involved in the modulation of SHH signaling, celi cycle regulation and canonical Wnt ligands, leading to impaired osteoblast function and reduction of bonę mass in Cd36-nuli mice. The exact mechanisms by which CD36 modulates bonę mass involve the crosstalk between several pathways. Futurę studies are needed to investigate further the relationship between CD36 and Wnt signaling molecules.

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