Fig. 1.

Human and mouse tandem pore domain acid-sensitive K⁺ (TASK) channels are associated with cardiac hypertrophy and heart failure. TASK-1 (A and C) and TASK-3 (B and D) gene expression in human and murine heart tissues. Human tissue (A and B) was obtained from subjects 1) without cardiac hypertrophy or heart failure (Normal), 2) with cardiac hypertrophy but without heart failure [left ventricular hypertrophy (LVH)], and 3) with both cardiac hypertrophy and heart failure [left ventricular hypertrophy and congestive heart failure (LVH & CHF)]. Murine tissue (C and D) was harvested from mice 1) without transverse aortic constriction (TAC) treatment (Sham), 2) 3 days after TAC, and 3) 7 days after TAC. KCNK3 and KCNK9, potassium two-pore domain channel subfamily K members 3 and 9, respectively; n = no. of mice or human tissue samples. Data are represented as fold change from Normal or Sham condition. Statistical comparisons with Normal, which has a theoretical mean of 1, were made with a one-sample t-test, *P < 0.05 vs. Normal or Sham. An unpaired t-test was employed to compare the differences between different conditions, †P < 0.05 vs. LVH or 7-day TAC. Mean raw ΔCt values (where Ct is threshold cycle; test Ct value minus housekeeping gene Ct value) ± SE. Comparisons between ΔCt values were made using a one-way ANOVA with Bonferroni’s test for multiple comparisons, †P < 0.05 vs. Normal or Sham.