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slightly larger in nuli mice, but was not statistically significant (data not shown). This mild alteration could involve CD36-dependent secretion of TNFa (Cai et al., 2012). Indeed, the TNF-a receptor 1 has been associated to new endochondral bonę formation in adult mice (Lukic et al., 2005). Moreover, TNF-a is known to induce leptin expression and secretion (Finek et Johnson, 2000); endochondral ossification of the Cd36-nuli mouse could therefore be delayed by lower leptin level.

Our data also show lower proliferative potential of Cd36-nuli MSCs, as reported previously in several other tissues (Ferracini et al., 2013; Vroegrijk et al., 2013; Woo et al., 2012; Won et al., 2008). Deletion of CD36 exacerbates injury after acute focal stroke in neonatal mice (Woo et al., 2012) and diminishes removal of apoptotic cells by macrophages (Ferracini et al., 2013). Cd36-nuli macrophages also show a decreased antigen-specific plasma celi generation with lower number of phosphoryl cholinę specific plasma cells (Won et al., 2008). CD36 deficiency promotes decreased adipocyte size in fat pads and impaired adipocyte reeruitment from precursor pools (Vroegrijk et al., 2013). The exact mechanisms by which CD36 regulates celi activity are still not fully elucidated. Celi cycle progression is crucial for both proliferation and differentiation; however, our results indicate that CD36 deficiency does not alter the percentage of MSCs in each celi cycle phase. The celi cycle is a multi-stage process, regulated by a variety of factors, such Cen, Ccn-dependent kinases and Ccn-dependent kinase inhibitors. The CcnD is essential for entry in G1 phase (Sherr, 1994), as CcnE and Cen A regulate progression from G1 into S phase (Ohtsubo et al., 1995). Some studies also revealed a relationship between the level of Cen A expression and apoptosis (Adachi et al., 2001; Rivera et al., 2006; Wang et al., 2009; Zuryn et al., 2007). Pro-apoptotic role of CcnA2 was shown in human erythroleukemie celi linę (Wang et al., 2009). Our results indicate inereased level of apoptosis in the adherent cells and greater number of neerotie cells in the supematant accompanied by augmented gene expression of CcnA2 and CcnDJ in Cd36-nuli MSCs. Along with the impaired proliferation, these data agree with the