Fig. 3.

MAP4 phosphorylation induces pathological cardiac hypertrophy. (a, b, c) Heart weight (HW), HW normalized by body weight (HW/BW) and HW normalized by tibia length (HW/TL) of two mouse models were determined. n = 10. (d) Heart histological sections with haematoxylin-eosin staining. Bar, 500 μm. n = 6. (e, f) FITC-WGA staining of LV heart sections, and cross sectional areas were analyzed in two mouse models. n = 6 (100 cells counted/animal). Bar, 20 μm. (g, h) Protein markers of hypertrophy in LV heart tissues were detected using WB analysis. n = 6. (i) Blood markers of cardiac damage from two mouse models were showed by cTnT and CK-MB. n = 9–11. (j) Representative TEM images showing ultrastructure of LV heart sarcomere (black circle represented myofilaments) between two mouse models. Bar, 2 μm. n = 6. (k, l) Protein markers of hypertrophy in CMs from two mouse models were detected with or without MAP4(Ala) transfection. n = 5. The experiment was conducted 5 times. (m) Cross sectional areas of CMs were analyzed by cTnI and FITC-WGA co-staining. n = 5. The experiment was conducted 5 times. ANP, atrial natriuretic peptide; MYH7, myosin heavy chain 7; BNP, brain natriuretic peptide; CMs, cardiomyocytes. Data were shown as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, ns, not statistically significant. P values were derived from one-way ANOVA with Bonferroni's post-test.