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. 2021 Dec 10;8:777098. doi: 10.3389/fcvm.2021.777098

Figure 6.

Figure 6

SLC37A2 deficiency impairs IL-4-induced macrophage activation in vitro. (A,B) SLC37A2 expression in WT and Slc37a2−/− bone marrow-derived macrophages (BMDMs) stimulated with 20 ng/ml IL-4 for 0-24 h. (A) relative transcript expression and (B) protein expression of SLC37A2 measured by qPCR and western blotting, respectively. (C) Relative transcript level of macrophage alternative activation markers, including arginase−1 (Arg), mannose receptor, type I (Mrc1), Ym1, IL-10, and chemokine MCP-1, in WT and Slc37a2−/− BMDMs stimulated with 20 ng/ml IL-4 for 0-24 h. (D,E) The relative transcript level of PPARs and genes encoding transporters or enzymes involved in fatty acid uptake or β-oxidation in WT and Slc37a2−/− BMDMs stimulated with 20 ng/ml IL-4 for 0-24 h. (F,G) Seahorse analysis of oxygen consumption rate (OCR) in WT and Slc37a2−/− BMDMs treated with or without 20 ng/ml IL-4 for 24 h. (H,I) Seahorse analysis of extracellular acidification rates (ECAR) in WT and Slc37a2−/− BMDMs treated with or without 20 ng/ml IL-4 for 24 h. Data are representative of two independent experiments with three samples per group (mean ± SEM). *p < 0.05; **p < 0.01; unpaired, two-tailed Student's t-test (A,C,D,E). Bars with different letters denote significant among groups (p < 0.05); two-way ANOVA with post hoc Tukey's multiple comparisons test (G,I).