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. 2017 Aug 11;16(5):1168–1179. doi: 10.1111/acel.12653

Figure 5.

Figure 5

Overexpression of valosin‐containing protein (VCP) significantly attenuated the angiotensin II (AngII)‐induced cardiomyocyte hypertrophy and the activation of the mTORC1 pathway in vitro. (A) The protein level of VCP in the neonatal rat cardiomyocytes (NRCMs) upon the transfection of adenovirus of VCP (Ad‐VCP) vs. Ad‐β‐Gal control with or without the presence of AngII. (B) The representative images of NRCMs stained by Troponin T. (C) The quantification data of NRCM surface area. (D) Western blots of proteins of AKT/mTORC1/S6K signaling in the NRCMs. GAPDH is a loading control for total protein. (E–H) The relative ratios of the corresponding proteins. *< 0.01 vs. vehicle. # < 0.01vs. β‐Gal‐AngII. NS: no significant difference. n = 4/treatment. Data are shown as mean ± SEM, two‐way ANOVA was used.