Figure 2

Aged Calstabin2-null mice display cardiac remodeling.

(A), Cardiac sections from young and old WT and KO mice were stained with hematoxylin-eosin. Bar = 100 μm. (B), mRNA levels of α-MHC, β-MHC, ANP and BNP were determined by real-time RT-qPCR. The expression of α-MHC was remarkably increased in cardiomyocytes from 6 week-and 12-week-old KO mice, respectively; whereas, the expression of ANP, BNP and β-MHC was significantly increased in 45- to 60-week-old KO mice compared to WT controls. (C), Representative Sirius red staining in transverse heart sections from young and aged Calstabin2 KO mice and WT littermate controls. Hearts from 48-week-old KO mice exhibited increased fibrosis. Bar = 25 µm. (12–15 fields of view were counted per each sample) (D), Representative images of terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining of heart sections from 12- and 48-week-old Calstabin2 KO mice and their littermates. As indicated by white arrows, aged Calstabin2 KO hearts exhibited significantly higher numbers of TUNEL-positive cells (arrows); Bar = 10 µm. (E), Quantification of cell death using TUNEL in the hearts of 12- and 48-week-old Calstabin2 KO and WT littermates (12–15 fields of view were counted per each sample) (F), Telomere length measured in young and aged hearts. (G), Quantitative real-time RT-qPCR products for miR-34a in hearts from 12 and 48-week-old Calstabin2 KO and WT littermates. Data are presented as the means ± s.e.m; n = 6 to 8 per group; *p < 0.05, **p < 0.01.