Figure 2: p38γ and p38δ control angiotensin II-induced hypertrophy.
From: p38γ and δ promote heart hypertrophy by targeting the mTOR-inhibitory protein DEPTOR for degradation
WT, p38γ−/−, p38δ−/− and p38γ/δ−/− mice were treated for 28 days with angiotensin II (AngII) (1 μg kg per minute) or saline, delivered by subcutaneously implanted osmotic minipumps. (a) Immunoprecipitation analysis of the phosphorylation and protein levels of p38γ and δ isoforms in heart extracts prepared from WT mice treated with AngII or saline. (b) Echocardiography results from AngII-treated WT, p38γ−/−, p38δ−/− and p38γ/δ−/− mice shown as the change relative to saline-treated controls. (c) Heart-weight-to-tibia-length ratios for WT, p38γ−/−, p38δ−/− and p38γ/δ−/− after 28 days of Ang II treatment. (d,e) Top: representative FITC-WGA staining (green) in hearts from 9-week-old WT, p38γ−/−, p38δ−/− and p38γ/δ−/− mice after AngII treatment. (e) Cardiomyocyte cross-sectional area quantified in WGA-stained hearts. (f) Echocardiography evaluation of systolic cardiac function increment after AngII treatment. IVS;d (inter-ventricular septum in diastole); LV (left ventricle). Data are means±s.e.m. (n=6–12). **P<0.01; ***P<0.001 (one-way analysis of variance coupled to Bonferroni post-tests); #P<0.05 (t-test between indicated groups).
