miR-210 in Exosomes Derived from Macrophages under High Glucose Promotes Mouse Diabetic Obesity Pathogenesis by Suppressing NDUFA4 Expression

Figure 3

miR-210 in exosomes derived from macrophages under high glucose inhibited adipocyte glucose uptake, CIV activity, and NDUFA4 expression. (a) Identification of miR-210 expression by RT-PCR assay in the treated Raw264.7 cells and exosomes derived from macrophages. Expression levels of miR-210 (b) and NDUFA4 gene (c) in 3T3-L1 cells treated with exosomes extracted from RAW-264.7 cells under high glucose after miR-210 inhibitor. miR-210 and NDUFA4 mRNA levels were analyzed by quantitative RT-PCR. (d) Glucose uptake by 3T3-L1 cells treated with exosomes from RAW-264.7 cells treated with miR-210 inhibitor under high glucose. Glucose content in 3T3-L1 cells was determined by the fluorometric method. (e) CIV activity in 3T3-L1 cells incubated with exosomes from RAW-264.7 cells with miR-210 inhibitor under high glucose. The ELISA method was used to analyze CIV activity. (f) NDUFA4 protein abundances in 3T3-L1 cells treated with exosomes derived from RAW-264.7 cells with silenced miR-210 expression under high glucose. VDAC1 was used as the internal standard. NG: normal glucose; HG: high glucose; NC: negative control; exo: exosomes; CIV: complex IV; NDUFA4: NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 4; VDAC1: voltage-dependent anion channel 1; (compared with the NC-normal glucose group); ^# and ^## (compared with the NC-high glucose group).

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