Fig. 5: Major metabolic tissues of Reg1cp-mutRIP+ mice obtained islets-derived exosomal Reg1cp and showed insulin resistance. | Cell Death & Disease

Fig. 5: Major metabolic tissues of Reg1cp-mutRIP+ mice obtained islets-derived exosomal Reg1cp and showed insulin resistance.

From: Mutated lncRNA increase the risk of type 2 diabetes by promoting β cell dysfunction and insulin resistance

Fig. 5

AF Representative pictures (A, C, E) and quantitative measurements (B, D, F) of western blot analysis of insulin stimulated IR, AKT, and GSK3β phosphorylation in liver (A, B), muscle (C, D) and epididymal white adipose tissue (eWAT, E, F) of Reg1cp-mutRIP+ mice and related Rosa-Reg1cp-mut controls. G Semi-quantitative PCR showed the expression level of Mut-Reg1cp in different tissues of Reg1cp-mutRIP+ mice. H Protein levels of Calnexin, CD9 and TSG101 in MIN6 cells or exosomes released by MIN6 cells. I Protein levels of TSG101, CD9 and CD63 in exosomes isolated from mice serum. J Semi-quantitative PCR showed the expression level of Mut-Reg1cp in exosomes isolated from Reg1cp-mutRIP+ mice serum, cultured medium of primary islets isolated from Reg1cp-mutRIP+ mice or cultured medium of MIN6 cells transfected with Mut-Reg1cp plasmids. K MIN6 cells derived exosomes were marked with red fluorescence dye PKH26 and then cocultured with 3T3-L1 adipocytes, C2C12 myocytes, and Hepa1-6 hepatocytes; Representative immunostaining images of PKH26 (red) and DAPI, nucleus (blue). Scale bar: 20 μm. In AF, n = 6 in each group from three independent experiments. GK were representative of two independent experiments. Data shown as mean ± SD. *P < 0.05; **P < 0.01; Student’s t test.

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