Fig. 4

KLK11 regulates cardiac hypertrophy in vivo. a KLK11 was knocked down in murine hearts with AAV9-mediated shRNA. n = 5 in each group. One week–old male C57BL/6 mice received a single intravenous injection of saline or AAV9 vector via the jugular vein. 12 weeks later, the mice received a TAC or sham surgery. The knockdown efficiency was confirmed by quantitative real-time PCR.***P < 0.001 by unpaired Student’s t test. AAV9, adeno-associated virus 9. b KLK11 knockdown rescues TAC-induced decline in fraction shortening and ejection fraction. One week–old male C57BL/6 mice received a single intravenous injection of saline or AAV9 vector via the jugular vein. Eight weeks later, the mice received a TAC or sham surgery. n = 8 in sham groups, n = 10 in TAC groups. **P < 0.01 by one-way ANOVA with Tukey post-hoc test. c KLK11 knockdown represses TAC-induced increase in heart weight to body weight ratio (HW/BW) and heart weight to tibia length ratio (HW/TL). One week–old male C57BL/6 mice received a single intravenous injection of saline or AAV9 vector via the jugular vein. Eight weeks later, the mice received a TAC or sham surgery. n = 8 in sham groups, n = 10 in TAC groups. **P < 0.01 by one-way ANOVA with Tukey post-hoc test. d Histochemical analysis showing KLK11 knockdown represses TAC-induced increase in cardiomyocyte size. One week–old male C57BL/6 mice received a single intravenous injection of saline or AAV9 vector via the jugular vein. Eight weeks later, the mice received a TAC or sham surgery. n = 8 in sham groups, n = 10 in TAC groups.**P < 0.01 by one-way ANOVA with Tukey post-hoc test. e KLK11 knockdown represses TAC-induced increase in hypertrophic genes. One week–old male C57BL/6 mice received a single intravenous injection of saline or AAV9 vector via the jugular vein, as previously described. Eight weeks later, the mice received a TAC or sham surgery. n = 8 in sham groups, n = 10 in TAC groups. **P < 0.01 by one-way ANOVA with Tukey post-hoc test