Fig. 4.
AAV9 mediated overexpression of circFndc3b improves cardiac function 8 weeks after MI in mice: a AAV9 vector expressing circFndc3b. b, c RT-qPCR analysis of precursor-circFNDC3b (n = 6 mice/group) and endogenous circFndc3b expression (n = 6 mice/group) in AAV9 circFndc3b or AAV9 control treated hearts at 8 weeks post MI. n = 5–7/group. *p < 0.05, ***p < 0.001 vs AAV9 control (two-sided unpaired students t-test); c, d RT-qPCR analysis of linear Fndc3b mRNA expression in AAV9 circFndc3b (n = 5 mice/group) or AAV9 control treated hearts (n = 6 mice/group) at 8 weeks post MI. Not significant (ns) vs AAV9 control (two-sided unpaired students t-test); f–i AAV9 mediated overexpression of circFndc3b (n = 7 mice) improved LV function (% ejection fraction, % fractional shortening, LVID; s and LVID; d measured by echocardiography compared to AAV9 control (n = 6 mice) or saline treatment groups (n = 5 mice). Data are Mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001 vs AAV9 control treated hearts. #p < 0.05, ##p < 0.01, ###p < 0.001 vs saline treated hearts, non-significant between saline and AAV9 control treated hearts (Two-way ANOVA). The round dots represent AAV9 control and square denotes AAV9-circFndc3b