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. 2015 Oct 5;125(11):4122–4134. doi: 10.1172/JCI82423

Figure 4. Genetic interaction of CIP and LMNA in dilated cardiomyopathy.

Figure 4

(A) H&E staining of 12-month-old Lmna+/– CIP-KO compound mice and their control littermates. Scale bar: 1.5 mm. (B) Progressive increase of LV internal dimension at end-diastole and decrease of FS in Lmna+/– CIP-KO mice from 6 to 12 months. (C) Survival curve of Lmna–/– CIP-KO mice and their control littermates. P < 0.05, for Lmna–/– vs. Lmna–/– CIP-Het; P < 0.05, for Lmna–/– vs. Lmna–/– CIP-KO, log-rank (Mantel-Cox) test. (D) Ratio between LV internal dimension at end-systole and tibial length (LVID;s/TL) and FS of Lmna–/– CIP-KO double mutant mice and their control littermates at the age of 5 weeks. (E) qRT-PCR detection of the expression of CIP and Lmna in CIP-KO and control hearts. (F) qRT-PCR detection of the expression of CIP in Lmna–/– and control (Lmna+/+) hearts. (G) Immunofluorescence images of CIP (CIP-GFP, GFP-tagged CIP), LMNA, and α-actinin in cardiomyocytes isolated from LMNA-KO and control (LMNA-WT) hearts. DAPI marked nuclei. Scale bar: 20 μm. (H) Immunoprecipitation of CIP and LMNA interaction. The n number for each group is indicated. *P < 0.05, **P < 0.01, 1-way ANOVA with post-hoc Tukey’s test.