Fig. 7.

Inhibition of MEK1/2 abolishes cardiac abnormalities in RGS14 ^−/− mice in response to pressure overload. a Representative western blotting and quantitative analysis of the phosphorylation levels of MEK1/2 and ERK1/2 in RGS14 ^−/− mice treated with an inhibitor of MEK (U0126) compared with DMSO in response to AB treatment (n = 4 mice per group). b–d The HW/BW, LW/BW, and HW/TL ratios in RGS14 ^+/+ and RGS14 ^−/− mice treated with U0126 or DMSO 4 weeks after AB surgery. (n = 9 for each group). e–g Echocardiographic parameters (LVEDd, LVESd, and FS%) for RGS14 ^+/+ and RGS14 ^−/− mice treated with U0126 or DMSO after AB surgery (n = 8–9 per group). h Sections of hearts from RGS14 ^+/+ and RGS14 ^−/− mice treated with U0126 or DMSO subjected to AB surgery were stained with H&E (first row: scale bar 50 μm) and PSR (second row and third row: scale bars 50 μm) to analyze cardiac hypertrophy and fibrosis (n = 5 per group). i Quantification of cardiomyocyte cross-sectional area in RGS14 ^+/+ and RGS14 ^−/− mice treated with U0126 or DMSO after AB surgery (n = 5 per group). j Quantification of fibrosis areas in RGS14 ^+/+ and RGS14 ^−/− mice treated with U0126 or DMSO after AB surgery (n = 5 per group). NS no significance. The data are presented as the mean ± SD