Figure 1. Loss of CIP accelerates the progress from hypertrophy to heart failure during cardiac remodeling.

(A) qRT-PCR detection of the expression of human CIP transcripts in the hearts of patients with dilated cardiomyopathy (DCM). n = 5–10 for each group. (B) Western blot detection of the expression of mouse CIP proteins in dilated cardiomyopathy and control mouse hearts. GAPDH was used as a control. (C) Expression of CIP mRNA (n = 3 for each group) and protein in CIP-KO hearts detected by qRT-PCR and Western blot, respectively. Arrowheads mark multiple CIP protein products encoded by CIP mRNA splicing isoforms. (D) LV internal dimension at end-diastole (LVID;d) and FS of CIP-KO and control mice at indicated ages. (E) Gross heart morphology and H&E staining of CIP-KO and control hearts 4 weeks after TAC or sham operation. Scale bar: 2 mm. (F) LV posterior wall thickness at end-diastole (LVPW;d), LV internal dimension at end-diastole, and FS of TAC- or sham-operated CIP-KO and control mice. (G) Heart cross sections were stained with wheat germ agglutinin, and cardiomyocyte cross-sectional area was quantified. Scale bar: 50 μm. (H) Fast green and Sirius red staining of TAC- or sham-operated CIP-KO and control hearts. The fibrotic area was quantified. Scale bar: 1.5 mm. (I) qRT-PCR detection of expression of hypertrophy marker genes. n = 3–5 for each group. *P < 0.05, **P < 0.01, 1-way ANOVA with post-hoc Tukey’s test. The n number for each group is indicated.