Fig. 5

KLK11 promotes protein synthesis. a KLK11 knockdown represses Ang II-induced protein synthesis in cardiomyocytes (n = 3). Mouse cardiomyocytes were transfected with siRNA for 24 h, followed by protein synthesis analysis by monitoring [³H]-leucine incorporation in the presence of Ang II (1 μM). ***P < 0.001 by one-way ANOVA with Tukey post-hoc test. b KLK11 overexpression promotes Ang II-induced protein synthesis in cardiomyocytes (n = 3). Mouse cardiomyocytes were infected with adenovirus for 24 h, followed by protein synthesis analysis by monitoring [³H]-leucine incorporation in the presence of Ang II (1 μM).. ***P < 0.001 by one-way ANOVA with Tukey post-hoc test. c KLK11 knockdown represses the phosphorylation of S6K1 and 4EBP1 in cardiomyocytes (n = 3). Mouse cardiomyocytes were transfected with siRNA for 24 h, followed by Ang II (1 μM) treatment for an additional 24 h. Representative western blots and quantitative results are shown. **P < 0.001 by one-way ANOVA with Tukey post-hoc test. d KLK11 overexpression promotes phosphorylation of S6K1 and 4EBP1 in mouse cardiomyocytes (n = 3). Mouse cardiomyocytes were infected with adenovirus for 24 h, followed by Ang II (1 μM) treatment for an additional 24 h. Representative western blots and quantitative results are shown. **P < 0.01 by one-way ANOVA with Tukey post-hoc test. e KLK11 knockdown represses the phosphorylation of S6K1 and 4EBP1 in vivo (n = 3). 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. Heart tissues from hypertrophic hearts with/without KLK11 knockdown were analyzed. Representative western blots and quantitative results are shown. **P < 0.01 by one-way ANOVA with Tukey post-hoc test