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Fig. 5 | Cell Communication and Signaling

Fig. 5

From: M1-derived extracellular vesicles polarize recipient macrophages into M2-like macrophages and alter skeletal muscle homeostasis in a hyper-glucose environment

Fig. 5

EVs from high glucose-treated macrophages modulate muscle homeostasis. A Quantification of insulin-induced phosphorylated AKT in C2C12 myotubes pre-treated with lEVs and sEVs from untreated , MG15, or MG30 macrophages. Data are expressed as ratios (pAKT/AKT)EV treated/(pAKT/AKT)untreated. Images of the blot are shown in Additional file 5. B Lipid droplets detected by Oil-O-Red in C2C12 myotubes pre-treated with lEVs and sEVs from untreated, MG15 and MG30 macrophages (scale bar = 40µm). C TLC analyses of neutral lipids, phospholipids, and sphingolipids of C2C12 myotubes treated with lEVs and sEVs from untreated, MG15 and MG30 macrophages. Significant lipid distributions were identified by a chi-squared test. TAG: triacylglycerol; FFA: free fatty acid; CHOL: cholesterol; PE: phosphatidylethanolamine; PC: phosphatidylcholine; PI+PS: phosphatidylinositol+phosphatidylserine; CER: ceramide; SS: sphingosine; SM: sphingomyelin. D mRNA level of interleukin 6 (Il-6) and (E) of transforming growth factor β (TGFβ), in C2C12 myotubes treated with lEVs and sEVs from untreated, MG15, and MG30 macrophages. Data are normalized to TBP mRNA level, then are expressed as fold of controls. Values are means ± SD (n = 3); p values are from student t-test (EV treated vs untreated), (*) p< 0.05, (**) p< 0.01, (***) p< 0.001

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