Skip to main content
. Author manuscript; available in PMC: 2019 Feb 1.
Published in final edited form as: J Mol Cell Cardiol. 2018 Jan 4;115:104–114. doi: 10.1016/j.yjmcc.2018.01.003

Figure 1. PKC inhibition protects against cardiac dysfunction and T-tubule remodeling following pressure overload.

Figure 1

A, Transient activation of PKC in mouse hearts induced by pressure overload. Administration of PKC inhibitor enzastaurin (Enz) abolished the transient activation of PKC. B–D, Summary data of heart weight/body weight ratio (HW/BW, B), lung weight/body weight ratio (LW/BW, C), and ejection fraction (EF, D) 5 wks after TAB or sham surgery. Some TAB mice were administered Enz, which attenuated the development of heart failure. n ≥ 6 mice/group. E, Representative left ventricular (LV) and right ventricular (RV) in situ confocal T-tubule images after staining with lipophilic marker MM4–64. F–I, Summary data in LV (F, G) and RV (H, I) of global T-tubule density (F, H) and the index of T-tubule integrity (TTint) (G, I). n=6, 10, 6 hearts for sham, TAB+DMSO and TAB+Enz, respectively. For each heart, 10 images were recorded from LV and RV, respectively. The analyzed outputs from the same heart were averaged to represent one heart. * p<0.05, ** p <0.01.