FIGURE 8.
miR-378 knockdown prevents the H2O2-induced apoptosis program and hypoxia/reoxygenation-induced cell death in an IGF1R-dependent manner. A, Western analysis (duplicates) of pIGF1R, IGF1R, and downstream signaling cascade in response to oxidative stress following transfection with either scramble control or 378-anti-miR. The same membrane was used again and again for probing with different antibodies after stripping. B, quantification of the signal intensity of A normalized essentially as described in the legend to Fig. 6E. C, time course response of TUNEL-positive nuclei in response to varying periods of hypoxia/reoxygenation in the presence of either scramble control or 378-anti-miR (50 nm). Each bar is a mean ± S.D. of a minimum of 3 independent experiments. D, quantification of TUNEL positive nuclei as described for the indicated treatment groups after 2 h of hypoxia followed by 2 h of reoxygenation injury to cardiac myocytes. The IGF1R inhibitor PQ-401(PQ) produced a dose-dependent inhibition of protective effects of 378-anti-miR. E, 378-anti-miR enhanced cardiomyocyte viability. Significant p < 0.05 (*) when compared with scramble control group and (#) when compared with the scramble PQ-treated group.