Fig. 1

Grpel2 was downregulated in the diabetic heart, and cardiac overexpression of Grpel2 attenuated the contractile dysfunction induced by STZ injection. A, B Western blotting and quantitative analysis of Grpel2 protein expression in the heart tissues of mice at 0, 6 and 12 weeks after vehicle or STZ injection (n = 4/group). C Quantitative real-time PCR of Grpel2 mRNA levels in heart tissues from mice at 0, 6 and 12 weeks after vehicle or STZ injection (n = 4/group). D Survival curve of mice intramyocardially injected with AAV9-Ctrl or AAV9-Grpel2 after vehicle or STZ injection (n = 16/group). E Representative short-axis M-mode echocardiographic images from mice intramyocardially injected with AAV9-Ctrl or AAV9-Grpel2 12 weeks after vehicle or STZ injection. F–L Quantification of left ventricular ejection fraction (LVEF, F), fraction shortening (LVFS, G), systolic internal dimension (LVISD, H), diastolic internal dimension (LVIDD, I), end-diastolic posterior wall thickness (LVPWd, J), end-systolic posterior wall thickness (LVPWs, K), and end-systolic posterior wall thickening (LVESWT, L) by short-axis M-mode echocardiography (n = 6–8/group). M Quantitative analysis of the early mitral diastolic wave/late mitral diastolic wave ratio (E/A ratio) by Doppler echocardiography (n = 6/group). Data are presented as the mean ± SD. Data in B and C were analysed with an unpaired, 2-tailed Student’s t test. Data in D were analysed with Log-rank Mantel-Cox testing. Other data were analysed by one-way ANOVA, followed by Tukey’s post hoc test. *p < 0.05