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

Figure 4.

Figure 4

Overexpression of Tsg101 in NRCMs promotes cell hypertrophy. A) Diagrams depicting the recombinant adenoviral vectors Ad.GFP and Ad.Tsg101. B) Representative images showing Ad.GFP- or Ad.Tsg101-infected NRCMs (left panel is under bright field; right panel is the same field under fluorescence microscope). Scale bars, 20 μm. C) Western blot showing increased expression of Tsg101 in Ad.Tsg101 cardiomyocytes compared with Ad.GFP cells. D, E) Measurement of myocyte cross-sectional area in those infected cells (green) that were stained with cardiomyocyte-specific α-actinin antibody (red). Scale bars, 20 μm. n = 6 plates, 25–30 cells per plate. F, G) Representative immunoblots (F) and quantitative analyses (G) showing expression of PM IGF-1R, total IGF-1R, Akt phosphorylation at Ser473, Rab5a, Rab4a, Rab7, Rab11a, and FIP3 in Ad.Tsg101 and Ad.GFP cells. GAPDH was used as loading control for total protein, total Akt was loading control for Akt phosphorylation, and Na/K-ATPase was loading control for PM protein. PM, plasma membrane; n = 4 for independent experiments. *P < 0.05 vs. Ad.GFP cells.