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Mobilization regulated by PPARd
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Figure 6. Function of ω3-fatty acids as PPARd ligands in vitro and in vivo. (A) Alteration of PPARd downstream genes by eicosapentaenoic acid (EPA)/docosa- hexaenoic acid (DHA) in sorted major myeloid populations from steady-state bone marrow (BM) in vitro and its interference by the PPARd antagonist GSK3787 (n=3- 5). (B) Modulation of granulocyte colony-stimulating factor (G-CSF)-induced mobilization by EPA administration in normal mice fed a fat-free diet (FFD) as assessed by white blood cells (WBC), lineage-Sca-1+c-kit+ (LSK) cells and colony-forming units in culture (CFU-C) in the blood (n=8). (C) Modulation of G-CSF-induced mobiliza- tion by EPA administration in chimeric mice with PPARd+/+ or PPARd+/- BM fed a FFD as assessed by WBC, LSK and CFU-C in the blood (n=4-6). The FFD was started 8 weeks after BM transplantation and G-CSF was started 2 weeks after the initiation of the FFD. Combined data from at least three independent experiments are shown. Data are mean ± standard error of mean. *P<0.05, **P<0.01, ***P<0.001 (Student t test and analysis of variance).
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