Figure 2.

Effects of acetylation-deficient p53^4KR on diastolic function, cardiac fibrosis, and apoptosis. A, Representative pulsed-wave Doppler and tissue Doppler images from an apical 4-chamber view of WT and p53^4KR mice subjected to either sham or TAC procedure for eight weeks and ratio of the peak velocity of early (E) to late (A) filling of mitral inflow (E/A) in the indicated groups (n=6–9). The ratio of E to the tissue motion velocity in early diastole (e’) was calculated in the indicated groups (n=6–10). B, Representative images of Picrosirius red-stained paraffin-embedded heart sections and quantification of the percentage of interstitial fibrosis area in the indicated groups (n=3–5). Bar=50 μm. C and D, Representative immunoblots and quantitative analysis of PDGFR-β, FSP-1, collagen-1, SERCA2 ATPase, α-tubulin, and GAPDH in the indicated mouse hearts (n=3–4 or 6–8). PDGFR-β and corresponding GAPDH were from the same membrane. FSP-1 and corresponding GAPDH were from the same membrane. SERCA2 ATPase and α-tubulin were from the same membrane. Collagen-1 and corresponding GAPDH were from different membranes. E, Representative images of TUNEL-stained frozen heart sections and quantification of the number of TUNEL-positive cells (green)/field in the indicated groups (n=4). 5–15 randomly selected fields per LV section of each mouse were measured. Bar=25 μm.