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. 2019 Mar 18;33(6):7451–7466. doi: 10.1096/fj.201802338RR

Figure 8.

Figure 8

Cardiac-specific KD of Tsg101 inhibits development of exercise-induced cardiac hypertrophy. A) Schematic showing the generation of cardiac-specific Tsg101-KD mice. B) Representative Western blot and quantification results showing Tsg101 protein levels in Tsg101-KD hearts compared with WTs. GAPDH was used as loading control. C, D) Representative immunoblots (C) and quantitative analysis (D) showing protein levels of FIP3, Rab11a, total IGF-1R, plasma membrane (PM) IGF-1R, and Akt phosphorylation in Tsg101-KD and WT hearts. GAPDH was loading control for total protein, total Akt was loading control for Akt phosphorylation, and Na/K-ATPase was loading control for PM-IGF-1R. E) Whole hearts and histologic sections stained with fluorescent-labeled WGA (scale bars, 20 μm) in sedentary and treadmill-trained WT and KD mice. Three constitutive sections of each heart were stained. F) HW:BW measurements in sedentary and treadmill-trained WT and KD mice. G) Quantification results for WGA staining of heart sections shown in E. EXE, treadmill-trained mice; SED, sedentary mice; n = 6 hearts for all groups. *P < 0.05 vs. WT-SED, #P < 0.05 vs. WT-EXE.