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. 2015 Feb 25;2(3):214–224. doi: 10.1016/j.ebiom.2015.02.013

Fig. 4.

Fig. 4

Effects of CLEC2 in vitro. (A–C) Activation of CLEC2 suppresses markers for M2 lineage of macrophage in vitro. (A) Anti-CLEC2 agonistic antibody induces strong aggregation of platelets. (B) Cultured RAW264.7 cells, treated with the CLEC2 agonistic antibody for 24 h, show significantly suppressed M2 marker, Arg1, but not M1 marker, Csf2. Antibody at 10 nM, LPS at 1 μg/ml, and IL4 at 100 ng/ml. amAb represents agonistic CLEC2 antibody. (C) Isolated peritoneal macrophages from 6 week old ob/ob animals show high expression of Clec2 but not other Clec molecules such as Clec5a, Clec7a, and Clec10a (***p < 0.001). (D) Fc-CLEC2(ECD) simulates liver oxidative phosphorylation and fatty acid oxidation in co-cultured Kupffer cells and primary hepatocytes. Co-cultured Kupffer cells and primary hepatocytes were treated with Fc-CLEC2(ECD) at a concentration of 200 ng/ml for 5 h. Fc-CLEC2(ECD) treatment induces expression of genes encoding components of oxidative phosphorylation (Ndufs, Sdhb) and fatty acid beta-oxidation (Acox1, Cpt1a), but not fatty acid transporters (Slc27a1). *p < 0.05, **p < 0.01, ***p < 0.001, one-way ANOVA. Results are expressed as the mean ± SEM and are representative of four independent experiments.