Fig. 4: TNF-α inhibits eNOS expression via NF-κB-dependent induction of miR-31/155. | Experimental & Molecular Medicine

Fig. 4: TNF-α inhibits eNOS expression via NF-κB-dependent induction of miR-31/155.

From: NF-κB-dependent miR-31/155 biogenesis is essential for TNF-α-induced impairment of endothelial progenitor cell function

Fig. 4

a The expression pattern of eNOS during the differentiation of CBMNCs into EPCs. b–e CBMNCs were stimulated with or without TNF-α (10 ng/ml) for the indicated time periods. Quantitative levels of miR-31 (b), miR-155 (c), eNOS mRNA (d), and eNOS protein and NO production (e) were determined by qRT-PCR, western blotting, and confocal microscopy (n = 4). **P < 0.01 and ***P < 0.001 vs. the initial control level. f, g CBMNCs were transfected with miRNA inhibitor negative control (NC) or miRNA inhibitors (miR-I; 31i, miR-31 inhibitor and 155i, miR-155 inhibitor), followed by treatment with TNF-α for 2 days. The levels of eNOS protein and NO production were determined by western blotting and confocal microscopy, respectively (n = 4). ***P < 0.001. h–j CBMNCs were transfected with AllStars negative control (NC or C), NF-κB p65 siRNA (sip65), or miR-31/155 mimics (31 m/155 m), followed by stimulation with TNF-α for 24 h. h–j The levels of miR-31 and miR-155 (h), eNOS protein (i), and NO production (j) were analyzed (n = 4). ***P < 0.001.

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